CLINICAL TRIALS

CLINICAL AFFILIATIONS

ASSOCIATIONS / MEMBERSHIPS

RESEARCH ABSTRACT

Overview of Contribution to Science. My research has been focused on the contribution of genetic and environmental factors in shaping immune response with a focus on autoimmunity. In search of potential genetic interactions between the host and the environment, we identified HRES-1, a human T-cell leukemia virus-related endogenous retrovirus (1), 将其定位到染色体1q42(2)上，并鉴定出Rab4a是其基因产物，通过增加表面受体的循环来调节易感性HIV感染, such as CD4 and transferrin receptor (CD71) (3). HRES-1内源性逆转录病毒的多态单倍型与SLE患者的发展和疾病表现相关(4). The overexpression of Rab4A gene product of HRES-1, which is detectable in T cells of SLE patients and in all lupus-prone strains prior to disease onset, also contributes to oxidative stress and mTOR activation by inhibiting mitochondrial turnover via autophagy, also called mitophagy (5). 这一新发现的狼疮发病途径也可以通过阻断Rab GTPases的酶活性来用于治疗干预, such as Rab4A using 3-PEHPC (5). The above discoveries have been published in 170 original peer-reviewed papers, authored chapters in rheumatology and immunology textbooks. Our work has been widely cited, credited, inspired a recent explosion of research on the role of metabolic pathways in the pathogenesis of lupus (6-9) and other rheumatic diseases (10,11).

我的实验室已经开辟了t细胞激活的代谢控制和谱系规范领域，这是小鼠模型和SLE患者疾病发展的基础,13). We have originally identified and cloned transaldolase, an enzyme of the pentose phosphate pathway (14), as a regulator of glutathione (GSH) metabolism (15,16)和一个新描述的t细胞活化和死亡信号处理的代谢检查点:线粒体跨膜电位或的升高, as newly termed, mitochondrial hyperpolarization (MHP) (17). As we also uncovered, persistent MHP is a critical metabolic defect in lupus T cells, which characterizes mitochondrial dysfunction and ATP depletion and predisposes to cell death by necrosis (18). 来自T细胞的坏死物质的增加是B细胞和树突状细胞的重要激活剂，并导致SLE的炎症(19)。. As we have also unveiled, the depletion of intracellular glutathione (GSH) underlies mitochondrial dysfunction and MHP in lupus T cells (18). To translate these new laboratory findings into clinical practice, we directly targeted the metabolic checkpoint of GSH depletion with N-acetylcysteine (NAC), an amino acid precursor of GSH, within the context of an FDA-approved double-blind placebo-controlled interventional trial (20). Relative to placebo, orally administered NAC reversed GSH depletion and showed remarkable safety, and it reduced disease activity in SLE patients (20,21). The clinical efficacy of NAC was mediated via blockade of complex 1 of the mechanistic target of rapamycin (mTOR), which serves as a sensor of MHP and effector of pro-inflammatory T cell lineage specification in SLE. As recently reviewed (13,22), the significance of mTOR activation is relevant for autoimmune diseases beyond SLE, it effects inflammation and overall lifespan. Based on our discovery of mTOR activation in SLE (23), 我们还评估了雷帕霉素的临床疗效，发现它对免疫抑制药物耐药或不耐受的SLE患者是一种非常有效的治疗干预, which has been repeatedly documented (22,24). Our findings on clinical efficacy of rapamycin have been corroborated by several recent publication, as recently reviewed (25).

Our parallel studies in mouse models led to the discovery of transaldolase (TAL) deficiency, as cause of inflammatory liver disease, which begins with steatohepatitis and progresses to hepatocellular carcinoma (HCC) (26). TAL deficiency has been documented as a cause of liver cirrhosis and cancer in patients as well, as recently reviewed (27). Interestingly, TAL is overexpressed in T cells of SLE patients, which may be related to protection against oxidative stress (23). The involvement of TAL in lupus pathogenesis is further supported by its increased expression in livers and spleen of MRL/lpr mice (28). Therefore, we examined whether oxidative stress, which emanates from the liver, can activate mTORC1 and thus predispose to aPL. Mitochondria from liver of mice lacking TAL (TAL-/-) exhibited increased electron transport chain (ETC) activity and activation of mTORC1. In accordance with an underlying role for oxidative stress and mTORC1 activation in the liver, the production of antiphospholipid antibodies (aPL) is increased in TAL-/- mice relative to TAL+/+ controls matched for age and gender. Importantly, 雷帕霉素治疗消除了TAL-/-小鼠抗心磷脂抗体(ACLA)和抗β2糖蛋白I自身抗体(抗β 2gpi)的产生. Likewise, aPL production was also blocked by rapamycin in lupus-prone mice (28).雷帕霉素在消除aPL产生方面的显著疗效与目前需要终身抗凝治疗的APS患者的治疗有着巨大的相关性(29)。.

Importantly, mild liver disease, defined as ≥2-fold elevation of aspartate aminotransferase or alanine aminotransferase, is associated with the production of aPL in our SLE cohort (30) as well as in previous meta-analyses (31,32). Along these lines, HCC develops in the liver following chronic inflammation, which is driven by mitochondrial oxidative stress (26,27) and responds to treatment with rapamycin (33). 越来越多的证据表明，雷帕霉素阻断mTORC1可以延长预期寿命(34)，这证明了这种干预的总体安全性和益处. Given that aPL may precede clinical disease in patients with SLE (35,36), 肝脏疾病的潜在作用和通过阻断mTORC1进行预防性治疗显然为研究和患者护理开辟了新的途径.

Of note, TAL is a rate-limiting enzyme of the pentose phosphate pathway (27). Deficiency of another PPP enzyme, glucose 6-phosphate dehydrogenase (G6PD), represents the most common genetic defect in humans, which affects 400 million people globally (37). Deficiency of G6PD elicits the depletion of NADPH in red cells and predisposes to oxidative stress-induced hemolytic anemia (37). The high prevalence of G6PD deficiency is attributed to its protective effects against malaria (38). In contrast to G6PD, TAL is not expressed in red cells, which lack mitochondria (39), and TAL deficiency does not cause hemolytic anemia in men or mice. However, the protozoan replicates in the liver, causes hepatitis(40,41) and induces aPL production (42). Therefore, the potential roles of TAL and the PPP as protectors from malaria would be important to determine.

As described in the above overview, my research has been dedicated to 1) uncovering the molecular basis of immune health, autoimmunity, and lupus pathogenesis and 2) identifying metabolic checkpoints of regulatory impact which can be validated in mechanistic clinical trials. To present specific discoveries and ongoing efforts, I have grouped them into four focused categories:

Research Projects

1. Discovery of the HRES-1 human endogenous retrovirus and the impact of its HRES-1/Rab4 gene product on T-cell activation and lupus pathogenesis

We have identified the HRES-1, the first human endogenous retrovirus (1) which is expressed on the RNA (1) and protein levels (43), exhibits polymorphic alleles conferring susceptibility to human lupus (44). HRES-1 is centrally located within the 1q42 locus associated with lupus susceptibility in 4 independent genome-wide screens of lupus families. Polymorphic haplotypes of HRES-1 are associated with the development of glomerulonephritis in SLE (4). HRES-1对SLE中T细胞信号传导改变的影响是通过HRES-1/Rab4蛋白介导的，HRES-1/Rab4蛋白通过内噬循环调节CD4的表面表达(3)。. HRES-1/Rab4 regulates assembly and recycling of key components of the T-cell synapse, including T-cell receptor/CD3ζ, and corresponds to the lupus susceptibility gene at 1q42 (23).HRES-1/Rab4A (recently designated by NCBI as Rab4A: http://www.ncbi.nlm.nih.gov/gene/5867) is markedly overexpressed in lupus T cells: 3.7-fold in CD4 T cells of SLE patients (23) as well as 3.6-fold in NZB/WF1 mice and 4.7-fold in MRL/lpr mice at 4 weeks of age, before the appearance of ANA or any sign of disease (5). As a member of the Ras-like Rab small GTPase family, HRES-1/Rab4regulates endosome recycling. In particular it targets the surface proteins CD4 (3), CD71 (transferrin receptor) (3), CD2AP, and CD3ζ (23) and the intracellular protein dynamin-related protein 1 (Drp1) for lysosomal degradation (5). Drp1 plays an essential role in triggering mitochondrial fission and mitochondrial autophagy (mitophagy) (45). Therefore, the HRES-1/Rab4-mediated depletion of Drp1 causes the accumulation of mitochondria, which generate oxidative stress, both in patients and mice with SLE (5). Of note, treatment with Rab GTPase inhibitor 3-PEHPC, which inactivates Rab4A in vitro, reverses the accumulation of mitochondria, blocks ANA production and nephritis in MRL/lpr mice in vivo (5). HRES-1/Rab4 increases the very formation of autophagosomes (46). 有人提出HRES-1/ rab4介导的自噬阻断可以阻止狼疮T细胞恢复T细胞激活诱导的代谢变化(47)。. Activation of endogenous retroviral elements, such as HRES-1 and LINE elements, contribute to the pathogenic interferon response in SLE (48). Such activation involves the accumulation of oxidative stress-generating mitochondria (5), oligomerization of the mitochondrial antiviral signaling protein (9), or sensing of retroviral RNA (48). Thus, pharmacological inactivation of Rab4A may represent a novel, mechanistic target for treatment of SLE.

2. 发现线粒体功能障碍和雷帕霉素(mTOR)作为SLE中促炎t细胞发展介质的机制靶点的激活

我们发现(首先)线粒体超极化(MHP)是T细胞活化和死亡的新检查点(17)，而狼疮T细胞中持续的线粒体超极化和线粒体生物发生增加与ATP消耗和细胞坏死死亡倾向有关(18)。. The release of necrotic materials is pro-inflammatory in SLE through potent activation of B cells and dendritic cells (19). 我们(首先)发现T细胞激活诱导的MHP是由一氧化氮(NO)引起的，一氧化氮是由人T细胞中一氧化氮合酶异构体eNOS和nNOS合成的(49)。. 持续的MHP和线粒体生物生成增加是由谷胱甘肽耗竭(18)和一氧化氮生成增强引起的，是SLE异常T细胞激活的基础(50)。. Since the mammalian target of rapamycin (mTOR) is a sensor of the Δψm in the outer mitochondrial membrane of T cells, we begun to use rapamycin for treatment of SLE patients resistant or intolerant to conventional immunosuppressants (24). 雷帕霉素有效控制SLE疾病活动性，使CD3/ cd28诱导的钙通量正常化，而不影响狼疮T细胞的MHP(24)。. This suggested that altered calcium fluxing is downstream or independent of mitochondrial dysfunction. Our most recent studies indicate a role for increased mTOR pathway activity in T cell dysfunction in SLE, by connecting mitochondrial dysfunction to enhanced calcium fluxing and altered formation of the immunological synapse (23). mTOR is a component of two interacting signaling complexes, mTOR complex 1 (mTORC1) and 2 (mTORC2). While mTORC1 is activated (5,20,23), mTORC2 is inhibited in lupus T cells (51). Such skewing may account for depletion of Tregs and expansion of effector T cells that produce IL-4 and IL-17 in SLE patients (22,51). mTORC1 activation contributes to the pathogenesis of SLE and related autoimmune diseases (13). Rapamycin elicits rapid, progressive, and sustained improvement of disease activity via correcting abnormal T-cell lineage specification in patients with active SLE (52). In particular, rapamycin blocked the activity of mTOR complex 1 in all T cells, expanded CD4+CD25+FoxP3+ regulatory, CD4+ central-memory (CD62L+CD197+), 和CD8+效应记忆(CD62L-CD197-) T细胞，并在12个月后抑制CD4-CD8-双阴性T细胞的促炎坏死和IL-4的产生(52)。. Unlike effector cells, Tregs of SLE patients exhibit deficient autophagy due to activation of an mTORC1/IL-21 positive feedback loop. Importantly, rapamycin treatment reverses deficient autophagy and facilitates the development and function of Tregs is patients with SLE (53).

在SLE和多发性硬化症患者中，线粒体DNA的非同义基因突变与疾病易感性之间的联系支持了线粒体功能障碍在自身免疫发病机制中的作用(54)。. 易感基因Sle1c2是通过雌激素相关受体γ (ESRRG)鉴定的，ESRRG是一种调节狼疮易感小鼠线粒体生物发生和介导CD4 t细胞高反应性的转录因子(6)。. 线粒体氧化应激诱导线粒体抗病毒信号蛋白(MAVS)寡聚化，从而触发SLE患者干扰素的产生(9)。.

Comprehensive metabolome analyses revealed an accumulation of pentose phosphate pathway (PPP) metabolites, depletion of cysteine, and the accumulation of kynurenine in lymphocytes of lupus patients relative to matched healthy controls (47). Kynurenine was identified as a metabolic trigger of mTORC1 activation and expansion of DN T cells (47). 我们有兴趣更好地定义人类和小鼠模型中产生氧化应激的线粒体积累和mTOR激活之间的串扰, including newly developed mice lacking HRES-1/Rab4 and the PPP enzyme, transaldolase.

由于电子传递链活性受阻而导致的线粒体功能障碍(55)以及由于线粒体自噬抑制而导致的线粒体积累(5)导致狼疮T细胞的氧化应激(12)。. In turn, oxidative stress activates mTORC1 (23,56,57) which can be effectively targeted for therapeutic intervention in SLE. We initiated two mechanistic clinical trials which are aimed at blocking the activation of mTOR complex 1 (mTORC1), directly by using rapamycin (22) and indirectly by using the antioxidant, N-acetylcysteine (20). Mitochondrial dysfunction and mTORC1 activation is also detectable in the liver of lupus-prone mice, which has been identified as an early event of disease pathogenesis that triggers the production of antiphospholipid autoantibodies (28). Given that mTOR activation has emerged as a biomarker and central pathway to autoimmune disorders, cancer, obesity and aging, personalized mTOR blockade holds promise to extend life span through preventing and foiling these conditions (58).

3. Discovery of transaldolase and its role in metabolic control of apoptosis, inflammation, autoimmunity, and progressive liver disease

人转醛缩酶(TAL)最初是在我们的实验室发现和克隆的(14)，并通过控制线粒体跨膜电位确定为程序性细胞死亡的代谢调节剂(15-17)。. Expression of transaldolase is controlled by an interplay between the transcription factors ZNF143 and AP2 (59). Transaldolase modulates the tissue-specific activity of the pentose phosphate pathway (27,59). The recently discovered genetic deficiency of transaldolase due to deletion of serin171 causes degradation of the enzyme in the proteasome (60). Transaldolase deficiency influences the pentose phosphate pathway, mitochondrial homeostasis, and apoptosis signal processing in human B cells (61). Transaldolase is cleaved and inactivated by granzyme B that may sensitize target cells to apoptosis induced by cytotoxic T cells (62). We have developed transaldolase-deficient mice that exhibit mitochondrial dysfunction in the sperm and some other cell types. 转醛dolase缺乏的雄性小鼠由于线粒体跨膜电位丧失和ATP产生减少而导致精子运动障碍而不育(63)。. Transaldolase-deficient mice spontaneously develop non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma (HCC) (26). NASH, cirrhosis, and HCC but not NAFLD are preventable by life-long treatment with N-acetylcysteine (26). These findings are relevant for the pathogenesis of chronic liver disease progressing from NAFLD to NASH, cirrhosis, and HCC in humans since transaldolase deficiency has already been documented in ten children, all with liver disease of varying severity. Mice deficient in transaldolase are also predisposed to acetaminophen/Tylenol-induced liver necrosis (26), the leading cause of acute liver failure in the US. Due to mitochondrial dysfunction and activation of mTORC1, Transaldolase deficiency predisposes to the production of antiphospholipid autoantibodies (28). Transaldolase-deficient mice are also susceptible to other autoimmune inflammatory diseases, which are currently being characterized (64).

4. Clinical research

To test the clinical relevance of our basic research findings, we have begun developing mechanistic clinical trials. We described first that rapamycin may be an effective treatment for lupus. We received investigator-initiated grant support from Wyeth, now Pfizer, 前瞻性研究雷帕霉素对40例狼疮患者整体基因表达和T细胞活化的影响以及临床结果.gov: IND No. 101,566). We are currently in discussion with NIAID about a follow-up randomized, placebo controlled trial with rapamycin in SLE. In addition, mTORC1 blockade with rapamycin may also benefit rheumatic diseases other than SLE (13). Our double-blind placebo-controlled study supported by NIH will determine the effect of NAC on glutathione depletion, mitochondrial hyperpolarization, and calcium signaling in lupus T cells and the clinical outcomes in SLE patients (clinicaltrials.gov: IND No 101,320). The 1st phase of our study double-blind placebo-controlled randomized study shows improved disease activity in NAC-treated SLE patients, relative to placebo, by reversing glutathione depletion and mTORC1 activation in T lymphocytes (20). 在本试验的背景下，我们还发现SLE患者表现出对NAC治疗有反应的注意缺陷和多动障碍症状升高(21)。. NAC may be beneficial for other co-morbidities of SLE, such as anti-phospholipid syndrome (65) and liver disease (30). To support the continuation of this study, a clinical trial center grant (UO1) and multicenter planning grant (U34) have been submitted to NIH. A grant award for planning of the multicenter trial has been issued by NIAMS for the period of 8/1/2016-7/31/2018. Application for planning a phase II mechanistic clinical trial to confirm preliminary results (52) is pending.

Reference List

PEER-REVIEWED SCIENTIFIC PUBLICATIONS:

1.  A.  Perl, B.  Fekete,  P.  Gergely, and  A.G.B.  Kovach (1982) Demonstration of Fc and C3b

receptors on rat perikarya. Acta Physiol. Hung. 60, 53‑56. PMID: 6223508

2.  A.  Perl, R.  Gonzalez‑Cabello, I.  Lang, and P. Gergely (1982) Depressed natural and lectin‑

dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells in patients with systemic lupus erythematosus. Immunol. Comm. 11, 431‑440. PMID: 7169224

3.  A.  Perl, E.  Pocsik, R.  Gonzalez‑Cabello, I.  Lang and P.  Gergely (1983) Human lectin‑

dependent T‑cell‑mediated cytotoxicity against HEp‑2 cells. Acta Physiol. Hung. 61, 225‑231. PMID: 6606296

4.  A.  Perl, R.  Gonzalez‑Cabello, I.  Lang, P. Somos and P. Gergely (1983) Depressed lectin‑

dependent cell‑mediated  cytotoxicity  against  adherent  HEp‑2 cells in patients with carcinoma of the uterine cervix. Cancer. Immunol. Immunother. 15, 155‑158. PMID: 6553513

5.  A.  Perl, R. Gonzalez‑Cabello, E. Pocsik, I. Lang and P. Gergely (1983) Effect of Fc receptor

blocking on human natural and lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Immunol. Letters, 6, 317‑321.  PMID: 6195101       

6.  A.  Perl, R.  Gonzalez‑Cabello and P.  Gergely (1983) Stimulation of lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells by carrageenan. Clin. Exp. Immunol. 54, 567‑572. PMID: 6652971; PMCID: PMC1535892

7.  E.  Pocsik,  R.  Gonzalez‑Cabello,  K.  Benedek, A.  Perl,  I.  Lang  and  P.  Gergely  (1983)

Characterization of the effector cells in Con A‑induced cytotoxicity against HEp‑2 tumour targets. Acta Med. Hung. 40, 41‑46. PMID: 6607455

8.  A. Perl, R. Gonzalez‑Cabello, I. Lang and P. Gergely (1984) Effector activity of OKT4+ and

OKT8+ T‑cell subsets in lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Cell. Immunol. 84, 185‑193. PMID: 6230158

9.  P.  Gergely,  K.  Nekam,  I.  Lang,  L.  Kalmar,  R.  Gonzalez‑Cabello and A. Perl (1984)

Ketoconazole   in   vitro   inhibits   mitogen‑induced   blastogenesis, antibody‑dependent cellular cytotoxicity,   natural    killer    activity    and    random    migration    of    human    leukocytes. Immunopharmacology, 7, 167‑170. PMID: 6088429

10.  A.  Perl, R.  Gonzalez‑Cabello and P. Gergely (1984) Depressed effector activity of OKT4+

和OKT8+ T细胞亚群在系统性红斑狼疮患者凝集素依赖性细胞介导的HEp - 2细胞毒性中的作用. J. Clin. Lab. Immunol. 15, 95‑100. PMID: 6240539

11. Lang I, Feuer L, Nekam K, Perl A, Szigeti A, Gergely P, Feher J. (1984) Effect of Litoralon therapy on the lymphocytotoxicity in patients with malignant tumors (In Hungarian). Orv. Hetil.

125:2193-2196. PMID: 6472845

12.  J.  Feher,  A.  Cornides,  A.  Vereckei,  I.  Lang,  K. Nekam, A. Perl and P. Gergely (1984)

Immunomodulatory effect of new radical scavengers. Drugs Expt. Clin. Res. X(8‑9) 549‑562.

13.   K.   Nekam,  I.  Lang,  L.  Kalmar, A. Perl  and  P.  Gergely  (1984)  Isoprinosine:  recent

experimental  and  therapeutic  results  with an antiviral immune modifier. Tissue Cult. Res, 173‑178.

14.  A. Perl, R. Gonzalez‑Cabello, K. Benedek, K. Nekam, I. Lang and P. Gergely  (1985) Effect

 of  histamin‑receptor  blocking  on  human  natural  and lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Thymus, 7, 111‑118. PMID: 4012822

15. A. Perl, R. Gonzalez‑Cabello, I. Lang and P. Gergely (1985) Depressed lectin‑dependent cell‑ mediated  cytotoxicity against  HEp‑2  cells in patients with different metastatic solid tumors. Acta Physiol. Hung. 65, 149‑153. PMID: 3872553

16.  A.  Perl, R.  Gonzalez‑Cabello,  L.  Falucskai, P.  Gergely, and J. Feher (1985) Contrasting

 effects of RNA and protein synthesis blocking on natural and lectin‑dependent cell‑mediated cytotoxicity against adherent HEp‑2 cells. Experientia, 41, 1344‑1346. PMID: 2412880

17.  A.  Perl,  R.  Gonzalez‑Cabello,  K.  Nekam,  P.  Gergely  and J Feher (1985) Stimulation by

thymopoietin  oligopeptides of lectin‑dependent cell‑mediated cytotoxicity in patients with systemic lupus erythematosus. J. Clin. Lab. Immunol. 18, 119‑122. PMID: 3910838

18.  A.  Perl,  I.  Lang,  R. Gonzalez‑Cabello, J. Filep, K. Nekam, P. Gergely and J Feher (1986)

Indomethacin   abrogates   the  suppression  by  cyclosporin  A  of  lectin‑dependent  cell‑mediated cytotoxicity to HEp‑2 cells. Immunopharmacology, 11, 39‑45. PMID: 3957649

19.  A.  Perl,  R.  Gonzalez‑Cabello,  T.  Laskay, M. Benczúr, I. Lang, K. Onody, K. Nekam, P.

Gergely and J Feher (1986) Lectin‑dependent cell‑mediated cytotoxicity and blastogenesis by LGL‑enriched and depleted lymphocytes. Clin. Exp. Immunol. 63, 171‑178. PMID: 3955881; PMCID: PMC1577327

20.  A.  Perl,  G. Repassy, R. Gonzalez‑Cabello, I. Lang and P. Gergely (1986) Depressed lectin‑

dependent  and  augmented  antibody‑dependent  cell‑mediated  cytotoxicity in patients with stage I cancer of the larynx. Natural Immunity and Cell Growth Regulation, 5, 100‑106. PMID: 3487714

21.  A.  Perl,  R.  Gonzalez‑Cabello,  K.  Onody, I. Bodo and P. Gergely (1986) Independence of

depressed  lectin‑dependent  cell‑mediated  cytotoxicity  from  interleukin‑2  production  in patients with systemic lupus erythematosus. Clin. Exp. Immunol. 65, 286‑292. PMID: 3491706

22.  A. Perl, A. Szigeti, P. Gergely, J. Feher, E. Magyarosi and M. Sellyei (1986) Abrogation by

chemotherapy  of  T‑cell  antigen  expression  in  B‑cell chronic lymphocytic leukemia. N. Engl. J. Med. 314, 186‑187. PMID: 2417119

23.  A.  Perl, R.J.  Looney, D.H.  Ryan and  G.N. Abraham (1986) The low affinity 40 kD Fc‑

gamma receptor and the transferrin receptor can be alternative or simultaneous target structures on cells sensitive for natural killing. J. Immunol. 136, 4714‑4720.

24.  T. Bakacs, K. Totpal, G. Ringwald, A. Perl and P. Gergely (1986) Quantitative determination of  anti‑A‑dependent  cytotoxicity  of  human  peripheral blood monocytes. J. Clin. Lab. Immunol. 19, 143‑147.

25. R. Gonzalez‑Cabello,  A.  Perl,  L.  Kalmar and P. Gergely (1987) Short‑term stimulation of

lymphocyte proliferation by indomethacin in vitro and in vivo. Acta Physiol. Hung. 70, 25‑30.

26.  J.  Feher,  I.  Lang,  Zs.  Pollak,  K.  Nekam,  R.  Gonzalez‑Cabello, A. Perl and P. Gergely

(1987)  Immunomodulatory and membrane protective effect of dihydroquinoline type antioxidants. In: Progress in Radio‑Oncology, Ed.: Karcher, K.H., ICRO, Vienna, pp. 218.

27.  K. Nekam, A. Perl, P. Gergely, R. Gonzalez‑Cabello and J. Feher (1987) Effect of dialyzable lymphocyte  extracts  on  lectin‑dependent cell mediated cytotoxicity in vitro. In Proceedings of the Fifth International Symposium on  Transfer  Factor.  Mayer  V. and Borvak J. (Eds.) Bratislava, Czechoslovakia.

28  I.  Lang,  K.  Nekam,  Gy.  Deak,  G.  Muzes,  R.  Gonzalez‑Cabello,  J.  Kadar, A. Perl, P.

Gergely  and  J.  Feher  (1987)  Effect  of  (+)cyanidanol‑3  on  cellular  immune reactions and on superoxide dismutase activity in vitro. Free Rad. Res. Comm. 4, 51‑60.

29.  A.  Cornides,  J.  Feher,  A. Perl, P. Gergely and A. Gogl (1987) Metronidazol induced liver

injury. Hepatology, 18, 11‑13.

30.  A.  Perl,  N. Wang, J.M. Williams, M.J. Hunt, S.I. Rosenfeld, J.J. Condemi, C.H. Packman

and  G.N.  Abraham  (1987)  Aberrant immunoglobulin and c‑myc gene rearrangements in patients with non‑malignant monoclonal cryoglobulinemia. J. Immunol. 139, 3512‑3520.

31.  A.  Perl,  P.D.  Gorevic,  D.H.  Ryan,  J.J.  Condemi,  R.J. Ruszkowski and G.N. Abraham

(1989)  Clonal  B‑cell  expansions  in  patients  with  essential mixed cryoglobulinemia. Clin. Exp. Immunol. 76, 54‑60.

32.  A. Perl, J.P. DiVincenzo, P. Gergely, J.J. Condemi and G.N. Abraham (1989) Detection and

mapping   of   polymorphic  KpnI  alleles  in  the  human  T‑cell  receptor  constant  beta‑2  locus. Immunology, 67, 135‑138.

33.  A.  Perl,  J.D.  Rosenblatt,  I.S.Y.  Chen, J.P. DiVincenzo, R. Bever , B.J. Poiesz, and G.N.

Abraham  (1989)  Detection  and  cloning  of  new HTLV‑related sequences in man. Nucleic Acids Res., 17, 6841‑6854.

34.  A.  Perl,  J.P.  Divincenzo,  D.H. Ryan, P. Gergely, A. Szigeti, J. Feher and G.N. Abraham

(1990)  Rearrangement  of the T‑cell receptor alpha, beta and gamma chain genes in B‑cell chronic lymphocytic leukemia. Leukemia Res. 14, 131‑137.

35.  G.N.  Abraham,  A.  Perl,  P.D.  Gorevic,  J.M.  Williams,  G. Jones, and R.A. Kyle (1990)

Molecular  genetic  analysis  of  human  monoclonal  gammopathies.  In: Biomedical  Advances  in Aging (Ed. A.L. Goldstein). Plenum Press, New York, pp. 355‑362.

36. Perl A, Feher J. Polymerase chain reaction in clinical diagnosis (In Hungarian). (1990) Orv. Hetil. 131:671-675.

37.  Perl, A.  (1990)  Role of a prostaglandin E1 analogue in prevention of acute graft rejection by cyclosporin A. N. Engl. J. Med., 323, 831‑832.

38.  A.  Perl,   K.  Nagy,  T.  Pazmany,  C. Isaacs, K. Baraczka, T. Szabo, & J. Feher (1990) No

evidence  for  HTLV‑I  or HTLV‑II infection in patients with multiple sclerosis. Arch. Neurol. 47, 1061‑1063.

39.  Perl,  A.,  Gorevic,  P.D.,  Condemi,  J.J.,  Papsidero,  L., Poiesz, B.J. and Abraham, G.N.

(1991)  Antibodies  to retroviral proteins and reverse transcriptase activity in patients with essential cryoglobulinemia. Arthritis. Rheum. 34, 1313‑1318.

40.  Perl, A., Isaacs, C.M.,  Eddy, R.L., Byers, M.G.,and Shows, T.B. (1991) The human T‑cell

leukemia  virus‑related  endogenous  sequence  (HRES‑1)  is  located  on  chromosome  1  at  q42. Genomics, 11, 1172‑1173.

41.  Banki,  K.,  J.S. Maceda, E. Hurley, E. Ablonczy, D. Mattson, L. Szegedy, C. Hung and A.

Perl  (1992)  HRES‑1, a human endogenous retroviral sequence encodes a 28 kd protein: a possible autoantigen for HTLV gag‑reactive autoantibodies. Proc. Natl. Acad. Sci. USA, 89, 1939‑1943.

42.  Krieg, A.M., Gourley, M.F. and Perl, A. (1992) Endogenous retroviruses: Potential etiologic

agents in autoimmunity. FASEB J. 6:2537‑2544.

43.  Srivastava, B.I.S., Banki, K. & Perl, A. (1992) Detection of human T‑cell lymphotropic virus type  I  or  a  related  retrovirus  in  patients  with mycosis fungoides, Sezary syndrome and Kaposi sarcoma. Cancer Res. 52, 4391‑4395.

44.   Krieg,  A.M.,  Gourley,  M.F.,  Klinman,  D.M.,  Perl,  A.,  and  Steinberg,  A.D.  (1992)

人内源性逆转录病毒序列在多发性肌炎患者和对照组外周血单核细胞中的异质表达和诱导.  AIDS Res. Hum. Retrovirus. 12, 1991‑1998.

45.  Perl, A. and Banki, K. (1993) Human endogenous retroviral elements and autoimmunity: data and concepts. Trends Microbiol. 1:153‑156.

46.  Agarwal, R.K. and Perl, A. (1993) PCR amplification  of highly GC‑rich DNA template after denaturation by NaOH. Nucleic Acids Res. 21, 5283‑5284.

47.  Banki,  K.,  Halladay, D. and Perl, A. (1994)人类转醛缩酶基因的克隆和表达:一个新的高度重复元件构成了编码序列的组成部分. J. Biol. Chem. 269:2847‑2851.

48.   Banki,   K.,   É.   Ablonczy,  M.  Nakamura,  and  Perl,  A.  (1994)  Effect  of  the  p40/tax

transactivator  of  human T‑cell lymphotropic virus type I (HTLV‑I) on expression of autoantigens. AIDS Res. Hum. Retrovirus 10:303-308.

49.  Magistrelli, C.,  Halladay, D., Agarwal, R., Ferrante, P., Perl, A. (1994) Mapping and cloning of polymorphic genotypes of the HRES-1 LTR. FASEB J. 8:A4395, manuscript in preparation.

50. Banki, K., E. Colombo, F. Sia, D. Halladay, D. H. Mattson, A.H. Tatum, P. T. Massa,  P. E. Phillips, Perl, A. (1994) Oligodendrocyte‑specific expression and autoantigenicity of transaldolase in multiple sclerosis. J. Exp. Med. 180:1649-1663.

51. Perl, A., Colombo, E., Dai, H., Agarwal, R.K., Mark, K., Banki, K., Poiesz, B.J., Phillips, P.E., Hoch, S.O., Reveille, J.D. and Arnett, F.C. (1995). 对HRES-1内源性逆转录病毒元件的抗体反应性鉴定了系统性红斑狼疮和重叠综合征患者的一个亚群:与抗核抗体和HLA II类等位基因的相关性. Arthritis Rheum. 38: 1660-1671.

52. Banki, K. and Perl, A. (1996) Inhibition of the catalytic activity of human transaldolase by antibodies and site-directed mutagenesis. FEBS Lett. 378: 161-165.

53. Banki, K., Hutter, E., Colombo, E., Gonchoroff, N.J. and Perl, A. (1996) Glutathione levels and sensitivity to apoptosis are regulated by changes in transaldolase expression. J. Biol. Chem. 271: 32994-33001.

54. Colombo, E., Banki, K., Tatum, A.H., Daucher, J., Ferrante, P., Murray, R.S., Phillips, P.E. and Perl, A. (1997)多发性硬化症患者对转醛缩酶和髓鞘碱性蛋白的抗体和细胞介导自身免疫的比较分析. J. Clin. Invest. 99:1238-1250.

55. Banki, K., Eddy, R.L., Shows, T.B., Halladay, D.L., Bullrich, F., Croce, C.M., Jurecic, V., Baldini, A. and Perl, A. (1997) The human transaldolase gene is located on chromosome 11 at p15.4-p15.5. Genomics, 45: 233-238.

56. Banki, K., Hutter, E., Gonchoroff, N.J. and Perl, A. (1998) Molecular ordering in HIV-induced apoptosis: oxidative stress, activation of caspases and cell survival are regulated by transaldolase. J. Biol. Chem. 273:11944-11953.

57. Banki, K., Hutter, E., Gonchoroff, N.J. and Perl, A. (1999)线粒体跨膜电位和ROI水平的升高是早期事件，独立于Fas信号中半胱天蛋白酶的激活. J. Immunol. 162:1466-1479. PMID: 9973403; PMCID: PMC4020419

58. Magistrelli, C., Samoilova, E., Agarwal, R.K., Banki, K., Ferrante, P., Vladutiu, A., Phillips, P.E. and Perl, A. (1999) HRES‑1人类内源性逆转录病毒位点的多态基因型与系统性红斑狼疮和自身反应性有关. Immunogenetics, 49:829-834.

59. Esposito, M., Venkatesh, V., Otvos,  L., Weng, Z., Vajda, S., Banki, K. and Perl, A. (1999) Human transaldolase and cross-reactive viral epitopes identified by autoantibodies of multiple sclerosis patients. J. Immunol. 163:4027-4032.

60. Perl, A. (1999) Mechanisms of viral pathogenesis in rheumatic diseases. Leader. Ann. Rheum. Dis. 58:454-461.

61. Perl, A., Colombo, E., Samoilova, E., Butler, M.C. and Banki. K. (2000) Human transaldolase-associated repetitive elements are transcribed by RNA polymerase III. J. Biol. Chem. 275:7261-7272.

62.  Puskas, F., Gergely, P. Jr., Banki, K. And Perl. A (2000) Stimulation of the pentose phosphate pathway and glutathione levels by dehydroascorbate, the oxidized form of vitamin C. FASEB J. 14: 1352-1361.

63. Thorell, S, Gergely, P.Jr., Banki, K. , Perl, A., Schneider, G. (2000) The three-dimensional structure of human transaldolase. FEBS Lett. 475:205-208.

64. Perl,  A., Banki, K. (2000) Genetic and metabolic control of the mitochondrial transmembrane potential and reactive oxygen intermediate production in HIV disease. Invited review. Antiox. Redox Signal., 2:551-573.

65. Perl, A. (2001) Editorial. Endogenous Retroviruses in Pathogenesis of Autoimmunity. J. Rheumatol. 28:461-464.

66. Lachaise, F., Martin, G., Drougard, C., Perl, A, Vuillaume, M., Wegnez, M., Sarasin, A., Daya-Grosjean, L. (2001)在紫外光敏感修复缺陷的着色性干皮病成纤维细胞和sv40转化的人类细胞中，翻译后醛缩酶修饰和过氧化氢酶缺乏的关系. Free Rad. Biol. Med. 30:1365-1373.

67. Perl, A. (2001) Abnormal Apoptosis in Systemic Lupus. Lupus News, 21:16-17.

68. Gergely, P. Jr., Grossman, C., Niland, B., Puskas, F., Neupane, H., Allam, F., Banki, K.,  Phillips, P.E. and Perl, A. (2002) Mitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosus. Arthritis Rheum. 46:175-190. PMID: 11817589

11817589; PMCID: PMC4020417

69. Puskas, F., Gergely, P., Niland, B., Banki, K. and Perl, A. (2002) Differential regulation of hydrogen peroxide and Fas-dependent apoptosis pathways by dehydroascorbate, the oxidized form of vitamin C. Antiox. Redox Signal. 4:357-369.

70. Perl, A,  Gergely, P., Puskas, F. and Banki, K. (2002) Metabolic switches of T cell activation and apoptosis. Antiox. Redox Signal. 4:427-443.

71. Kammer, G.M., Perl, A., Richardson, B.C., Tsokos, G.C. (2002) Abnormal T cell signal transduction in systemic lupus erythematosus. Arthritis Rheum. 46:1139-1154.

72. Gergely, P. Jr., Niland, B., Gonchoroff, N., Pullmann, R. Jr., Phillips, P.E. and Perl, A.(2002) Persistent mitochondrial hyperpolarization, increased reactive oxygen intermediate production, and cytoplasmic alkalinization characterize altered IL-10 signaling in patients with systemic lupus erythematosus. J. Immunol. 169:1092-1101.

73. Nagy, Gy, Koncz, A. and Perl A (2003) T cell activation-induced mitochondrial hyperpolarization is mediated by Ca²⁺- and redox-dependent production of nitric oxide. J. Immunol. 171:5188-5197.

74.  Mukhopadhyay, S., Mousa, S., George, B.R. and Perl, A. (2004) Palpable purpura, polyarthritis, and abdominal pain. Med. J. Aust. 180:121-122.

75. Perl, A., Gergely, P. Jr., Nagy, G., Koncz, A., and Banki, K. (2004). Mitochondrial hyperpolarization: a checkpoint of T-cell life, death, and autoimmunity. Trends Immunol. 25:360-367.

76. Grossman, C. E., Qian, Y., Banki, K., Perl, A. (2004) ZNF143 mediates basal and tissue-specific expression of human transaldolase. J. Biol. Chem. 279: 12190-12205.

77. Perl,A.; Gergely,P.,Jr.; Banki,K. (2004) Mitochondrial dysfunction in T cells of patients with systemic lupus erythematosus. Int. Rev. Immunol. 23:293-313.

78. Grossman, C. E., Niland, B., Stancato, C, Verhoeven, N.M., van der Knaap, M.S., Jakobs, C., Brown, L.M.,  Vajda, S., Banki, K.  and  Perl, A. (2004) Deletion of serine 171 causes inactivation, proteasome-mediated degradation and complete deficiency of human transaldolase. Biochem. J. 382:725-231.

79. Nagy, Gy, Barcza. M., Gonchoroff, N., Phillips, P.E. and Perl, A. (2004) Nitric oxide-dependent mitochondrial biogenesis generates Ca²⁺ signaling profile of lupus T cells. J. Immunol. 173:3676-3683. PMID: 15356113; PMCID: PMC4034140

80. Nagy, Gy, Koncz, A, Phillips, P.E. and Perl, A. (2005) Mitochondrial signal transduction abnormalities in systemic lupus erythematosus. Curr. Immunol. Rev. 1: 61-67.

81. Gergely. P. Jr,  Pullmann, R., Stancato, C., Otvos, L. Jr, Koncz, A., Blazsek, A., Poor, Gy,  Brown, K.E., Phillips, P.E. and Andras Perl^. (2005)在系统性红斑狼疮患者中，输血传播病毒的流行率和HRES-1/p28内源性逆转录病毒自身抗原免疫显性表位的交叉反应性增加. Clin. Immunol. 116: 124-134.

82. Nagy, Gy, Koncz, A, and Perl, A. (2005) T- and B-cell abnormalities in systemic lupus erythematosus. Crit. Rev. Immunol. 25: 123-140.

83. Nagy, Gy, Koncz, A, and Perl, A. (2005) Signal transduction abnormalities in systemic lupus erythematosus (In Hungarian). Orv. Hetil. 146:1625-1630.

84. Niland, B., Banki, K., Biddison, W.E. and Perl, A. (2005) CD8+ T cell-mediated HLA-A*0201-restricted cytotoxicity to transaldolase peptide 168-176 in patients with multiple sclerosis. J. Immunol. 175: 8365-8378.

85. Quintero M, Mirza N, Chang H, Perl A. (2006) Antiphospholipid antibody syndrome associated with primary angiitis of the central nervous system: report of two biopsy-proven cases. Ann. Rheum. Dis. 65 :408‑9

86. Nagy G. and Perl, A. (2006) The role of nitric oxide in abnormal T cell signal transduction in systemic lupus erythematosus. Clin. Immunol. 118: 145-151.

87. Vas, Gy., Conkrite, K., Amidon, W., Qian, Y., Banki, K., and Perl, A. (2006) Study of transaldolase deficiency in urine samples by LC-MS/MS. J. Mass. Spec. 41: 463-469.

88. Fernandez, D., Bonilla, E., Mirza, N, Niland, B. and Perl, A. (2006) Rapamycin reduces disease activity and normalizes T-cell activation-induced calcium fluxing in patients with systemic lupus erythematosus. Arthritis Rheum. 54: 2983-2988. PMID:16947529; PMCID: PMC4034146

89. Perl, A., Qian, Y, Chohan, K.R., Shirley, C.R., Amidon, W., Banerjee, S., Middleton, F.A., Conkrite, K.L., Barcza, M., Gonchoroff, N., Suarez, S.S., and Banki, K. (2006) Transaldolase is essential for maintenance of the mitochondrial transmembrane potential and fertility of spermatozoa. Proc. Natl. Acad. Sci. USA, 103: 14813-14818. PMID:17003133; PMCID: PMC1595434

90. Nagy, G., Ward, J., Mosser, D.D., Koncz, A., Gergely, P. Jr., Stancato, S., Qian, Y, Fernandez, D., Niland, B., Grossman, C.E., Telarico, T, Banki, K, Perl, A. (2006) Regulation of CD4 expression via recycling by HRES‑1/RAB4 controls susceptibility to HIV infection. J. Biol. Chem. 281: 34574-34591. PMID:16935861

91. Fernandez, D., Bonilla, E., Phillips, P.E. and Perl, A. (2006)  Signaling abnormalities in systemic lupus erythematosus as potential drug targets. Endocrin, Metabolic & Immune Disorders - Drug Targets. 6: 305-311.

92. Gergely, P., Perl, A. and Poor, Gy. (2006) Possible pathogenic nature of the recently discovered TT virus.  Does it play a role in autoimmune rheumatic diseases? Autoimmun. Rev. 6:5-9.

93. LaRocca, D., Lehmann, D.F., Perl, A., Ozawa, T., Holohan, P. D. (2006) The combination of nuclear and mitochondrial mutations as a risk factor for idiosyncratic toxicity. Brit. J. Clin. Pharm. 63:249-251.

94. Silberstein, M., Landon, M.R., Wang, Y.E., Perl, A. and Vajda, S. (2006) Computational methods for functional site identification suggest a substrate access channel in transaldolase. Genome Inform. 17: 13-22.

95. Koros, A., Hanczko, R., Jambor, Qian, Y., Perl, A. and Molnar-Perl, I. (2007) Analysis of amino acids and biogenic amines in biological tissues as their o-phthalaldehyde/ethanethiol/fluorenylmethyl chloroformate derivatives by high-performance liquid chromatography: A deproteinization study. J. Chromatogr. A 1149: 46-55.

96. Nagy, G., Koncz, A., Fernandez, D. and Perl A. (2007). Nitric oxide, mitochondrial hyperpolarization, and T-cell activation. Free Radic. Biol. Med. 42: 1625-1631.

97. Perl, A. (2007) The pathogenesis of transaldolase deficiency. IUBMB Life 59: 365-373.

98. Bonilla, E., Francis, L., Allam, F., Ogrinc, M., Neupane, H., Phillips, P.E., and Perl, A. (2007)免疫荧光显微镜检测系统性红斑狼疮患者的抗核抗体反应性优于荧光珠. Clin. Immunol. 124:18-21.

99. Hanczko, R., Jambor, A., Perl, A., and I Molnar-Perl (2007) Advances in the o-phthalaldehyde derivatizations: Comeback to the o-phthalaldehyde-ethanethiol reagent. J. Chromatogr. A 1163: 25-42.

100. Bonilla, E., Lee, Y.Y., Phillips, P.E., and Perl, A. (2007) Hypoglycaemia after initiation of etanercept treatment in a patient with type 2 diabetes mellitus. Ann. Rheum. Dis. 66:1688.

101. Pullmann, R. Jr., Bonilla, E., Phillips, P.E., Middleton, F.A. and Perl, A. (2008) Haplotypes of the HRES-1 endogenous retrovirus are associated with development and disease manifestations of systemic lupus erythematosus. Arthritis Rheum. 58: 532-540. PMID: 18240231

102. Francis L, Bonilla E, Soforo E, Neupane H, Nakhla H, Fuller C, and Perl A. (2008) Fatal toxic myopathy attributed to propofol, methylprednisolone, and cyclosporine after prior exposure to colchicine and simvastatin. Clin. Rheumatol. 27:129-31.

103. Perl, A., Nagy, G., Koncz, A., Gergely, P., Fernandez, D., Doherty, E., Telarico, T., Bonilla, E. and Phillips, P.E. (2008) Molecular mimicry and immunomodulation by the HRES-1 endogenous retrovirus in SLE. Autoimmunity, 41:287-297. PMID: 18432409PMID:18432409

DOI: 10.1080/08916930802024764

104. Qian, Y., Banerjee, S., Grossman, C.E., Amidon, A., Nagy, Gy., Barcza, M., Niland, B.,  Karp, D.R., Banki, K., and Perl, A. (2008) Transaldolase deficiency influences the pentose phosphate pathway, mitochondrial homeostasis, and apoptosis signal processing. Biochem. J. 415:123-134.

105. Vyshkina, T., Sylvester, A., Sadiq, S., Bonilla, E., Canter, J., Perl, A. and Kalman, B.(2008) Association of Common Mitochondrial DNA Variants with Multiple Sclerosis and Systemic Lupus Erythematosus. Clin. Immunol. 129:31-35.

106. Vyshkina, T., Sylvester, A., Sadiq, S., Bonilla, E., Perl, A. and Kalman, B.(2008) CCL genes in multiple sclerosis and systemic lupus erythematosus. J. Neuroimmunol. 200:145-152.

107. Perl, A. (2009) Overview of Signal Processing by the Immune System in SLE. Autoimmun. Rev. 8:177-178.

108. Fernandez D.R. and  Perl, A. (2009) Metabolic control of T-cell activation and death in SLE. Autoimmun. Rev. 8:184-189.

109. Fernandez, D.R. Telarico, T., Bonilla, E., Li, Q., Banerjee, S., Middleton, F.A., Phillips, P.E.,  Crow, M.K., Oess, S., Muller-Esterl, W., and Perl, A. (2009) Activation of mTOR controls the loss of TCRζ in lupus T cells through HRES-1/Rab4-regulated lysosomal degradation. J. Immunol. 182: 2063-2073. PMID:19201859; PMCID: PMC2676112

110. Hanczko, R., Fernandez, D.R., Doherty, E.,  Qian, Y., Vas, G., Niland, B., Telarico, T., Garba, A., Banerjee, S., Middleton, F.A., Barrett, D., Barcza, M., Banki, K., Landas, S.K. and Perl, A. (2009) n-乙酰半胱氨酸预防对乙酰氨基酚诱导的转醛dolase缺陷小鼠肝癌发生和增加对乙酰氨基酚诱导的肝衰竭易感性. J. Clin. Invest. 119:1546-1557. PMID: 19436114; PMCID: PMC2689120

111. Francis, L. and Perl. A. (2009) Pharmacotherapy of SLE. Expert Opin. Pharmacother. 10: 1481-1494.

112. Perl, A., Fernandez, D., Telarico, T., Francis, L. and Phillips, P.E. (2009) T- and B-cell signaling biomarkers and treatment targets in lupus. Curr. Opin. Rheumatol. 21: 454-464.

113. Perl, A. (2009) Editorial: Emerging New Pathways of Pathogenesis and Targets for Treatment in Systemic Lupus Erythematosus and Sjogren's Syndrome. Curr. Opin. Rheumatol. 21: 443-447.

114. Bedoya, F.,  Medveczky, M.M.,  Lund, T.C., Perl, A., Horvath, J., Jett, S.D. and Medveczky, P.G. (2009) Identification of Mitochondrial Genome Concatamers in AIDS-associated lymphomas and lymphoid cell lines. Leuk. Res. 33:1499-1504.

115. Tily, HI and Perl, A. (2009) Lymphedema: a paradoxical effect of tumor necrosis factor inhibitors - case report and review of literature. BMJ Case Reports [doi:10.1136/bcr.07.2008.0520]

116. Blank, M., Shoenfeld, Y. and Perl, A. (2009) Cross-talk of the environment with the host genome and the immune system through endogenous retroviruses in systemic lupus erythematosus. Lupus, 18: 1136-1143.

117. Soforo, E., Baumgartner, M., Francis, L., Allam, F., Phillips, P.E., and Perl, A. (2010) Induction of systemic lupus erythematosus with TNF blockers. J. Rheumatol. 37:204-205.

118. Francis, L. and Perl. A. (2010) Infection in systemic lupus erythematosus: friend or foe? Int. J. Clin. Rheumatol. 5:59-74.

119. Perl, A. (2010) Editorial: Pathogenic Mechanisms in Systemic Lupus Erythematosus. Autoimmunity, 43:1-6.

120. Perl, A. (2010) Systems biology of lupus: mapping the impact of genomic and environmental factors on gene expression signatures, cellular signaling, metabolic pathways, hormonal and cytokine imbalance and selecting targets for treatment. Autoimmunity 43: 32-47.

121. Tily, H., Banki, K., Hoffman, G.S. and Perl. A. (2010) Detection of lupus anti-coagulant and successful anti-coagulation in familial Sneddon syndrome. Ann. Rheum. Dis. 69: 775-776.

122. Niland, B, Miklossy, G,  Banki, K, Biddison, W.E.,  Casciola-Rosen, L., Rosen, A.,  Martinvalet, D., Lieberman, J., and Perl, A. (2010)在多发性硬化症患者中，颗粒酶B切割转醛缩酶导致酶活性丧失，但保留了抗原性. J. Immunol., 184:4025-32.

123. Perl, A., Fernandez, D., Telarico, T, and Phillips P.E. (2010). Endogenous retroviral pathogenesis in lupus. Curr. Opin. Rheumatol. 22:483-492.

124. Nagy, G., Koncz, A., Telarico, T., Fernandez, D., Ersek, B., Buzas, E., and Perl, A. (2010) Central role of nitric oxide in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus. Arth. Res. Ther. 12:N. (http://arthritis-research.com/content/12/3/N)

125. Engelke, Udo F.H., Fokje S.M. Zijlstra, Fanny Mochel, Vassili Valayannopoulos, Daniel Rabier, Leo A.J. Kluijtmans, Andras Perl, Nanda Verhoeven-Duif, Pascale de Lonlay-Debeney, Mirjam M. Wamelink, Cornelis Jakobs, Éva Morava, Ron A. Wevers. (2010) Erythronic Acid as a Novel Biomarker in Transaldolase Deficiency. Biochim. Biophys. Acta  - Molecular Basis of Disease. 1802 (11):1028-1035.

126. Fernandez, D. and Perl, A. (2010) mTOR Signaling: A Central Pathway to Pathogenesis in Systemic Lupus Erythematosus? Discov. Med.  9:173-178.

127. Hernández-Negrete, I, Sala-Newby, G.B., Perl, A, Kunkel, G.R., Newby, A.C. and Bond, M.(2011) Adhesion-dependent SKP2 transcription requires selenocysteine tRNA gene transcription activating factor (STAF). Biochem. J. 436:133-143.

128. Perl, A. (2011) Deleterious effects of TNF blockade in SLE. J. Rheumatol. 38:1217.

129. Perl, A., Hanczko, R., Telarico, T., Oaks, Z. and Landas S. (2011). Control of oxidative stress, inflammation, and carcinogenesis through the pentose phosphate pathway by transaldolase. Trends Mol. Med. 17: 395-403. PMID: 21376665

130. Sreih, A., Ezzeddine, R., Leng, L., Lachance, A., Yu, G., Mizue, Y., Pons-Estel, B., Abelson, A-K.,  Gunnarsson, I., Svenungsson, E., Cavett, J., Glenn, S., Zhang, L., Montgomery, R., Perl, A., Salmon, J., Alarcon-Riquelme, M., Harley, J.B., Bucala, R. (2011) Dual Effect of Macrophage Migration Inhibitory Factor Gene on the Development and the Severity of Human Systemic Lupus Erythematosus. Arthritis Rheum. 63: 3942-3951.

131. Talaber, G. and Perl, A. (2011) SLE: a Metabolic Disease of T Cells? OMICS Rheumatology 1:e103. http://dx.doi.org/10.4172/2161-1149.1000e103

132. Talaber G, Perl A (2012) The molecular pathogenesis of SLE. Immunolologia Szemle (Immunological Quarterly, Hungarian with English abstract) 1:4-11

133. Perl, A. (2012) Editorial. Oxidative stress and endosome recycling are complementary mechanisms reorganizing the T-cell receptor signaling complex in SLE. Clin. Immunol. 142: 219-222.

134. Perry, D.J., Yin, Y, Telarico, T., Baker, H.V., Dozmorov, I, Perl, A. and Morel, L. (2012) Murine Lupus Susceptibility Locus Sle1c2 Mediates CD4⁺ T cell Activation and Maps to Estrogen-Related Receptor Gamma Esrrg. J. Immunol. 189: 793-803. PMID: 22711888 22711888; PMCID: PMC3392454

135. Caza, T.N., Talaber, G. and Perl, A. (2012) Metabolic regulation of organelle homeostasis in lupus T cells. Clin. Immunol. 144: 200-213. PMID: 22836085

136. Meszaros, Z., Perl, A, Faraone, S. (2012) Psychiatric symptoms in systemic lupus erythemathosus. J. Clin. Psych. 73: 993-1001. PMID:22687742

137. Lai, Z-W, Hanczko, R., Bonilla, E, Caza, T.N., Clair, B., Bartos, A., Miklossy, G, Jimah, J., Doherty, E, Tily, H., Francis, L, Garcia, R., Dawood, M., Yu, J., Ramos, I., Coman, I., Faraone, S.V., Phillips, P.E. and Perl, A. (2012). N-acetylcysteine reduces disease activity by blocking mTOR in T cells of lupus patients. Arthritis Rheum. 64: 2937-2946. PMID: 22549432; PMCID: PMC3411859

138. Alessandri, C, Barbati, C., Vacirca, D., Piscopo, P., Confaloni, A.M., Maselli, A., Colasanti, T., Conti, F., Truglia, S., Perl, A., Valesini, G, Ortona, E., Malorni, W, and Pierdominici, M. (2012) T lymphocytes from patients with Systemic Lupus Erythematosus are resistant to induction of autophagy. FASEB J. 26: 4722-4732. PMID: 22835828;  PMCID: PMC3475261

139. Garcia, R.J., Francis, L., Dawood, M, Lai, Z-W., Faraone, S.V., and Perl, A. (2013) Attention Deficit and Hyperactivity Disorder Scores are Elevated and Respond to NAC treatment in patients with SLE. Arthritis Rheum. 65: 1313-1318. PMID: 23400548

140. Singh N, Birkenbach M, Caza T, Perl A, Cohen PL. (2013) Tuberous sclerosis and fulminant lupus in a young woman.  J. Clin. Rheumatol. 19(3):134-7. doi: 10.1097/RHU.0b013e318289c033. PMID: 23519178

141. Gilkeson GS, Mashmoushi AK, Ruiz P, Caza TN, Perl A, and Oates JC. (2013) Endothelial Nitric Oxide Synthase Reduces Crescentic and Necrotic Glomerular Lesions, Reactive Oxygen Production, and MCP1 Production in Murine Lupus Nephritis. PLoS ONE 8(5): e64650. doi:10.1371/journal.pone.0064650 PMID: 23741359

142. Lai, Z-W, Borsuk, R., Shadakshari, A., Yu, J., Dawood, M., Garcia, R., Francis, F., Tily, H., Bartos, A., Faraone, S.V., Phillips, P.E. and Perl. A. (2013). mTOR activation triggers IL-4 production and necrotic death of double-negative T cells in patients with systemic lupus eryhthematosus. J. Immunol. 191: 2236-2246. doi: 10.4049/jimmunol.1301005. PMID: 23913957

143. Perl, A. (2013) Oxidative stress in the pathology and treatment of systemic lupus erythematosus. Nat. Rev. Rheumatol. 9:674-686. PMID: 24100461

144. Caza, T.N., Fernandez, D.R., Talaber, G., Oaks, Z., Haas, M., Madaio, M.P., Lai, Z-W, Miklossy, G.,  Singh, R.R., Chudakov, D.M., Malorni, W., Middleton, F., Banki, K, and Perl, A. (2014) HRES-1/RAB4-mediated depletion of Drp1 impairs mitochondrial homeostasis and represents a target for treatment in SLE. Ann. Rheum. Dis. 73:1888-1897. PMID:23897774; PMCID:PMC4047212

145. Oaks, Z. and Perl, A. (2014). Metabolic control of the epigenome in systemic lupus erythematosus. Autoimmunity, 47:256-264. PMCID: PMC4034124

146. Fali, T, Le Dantec, C, Thabet, Y., Jousse, S., Hanrotel, C., Brooks, W.H., Perl, A., and Renaudineau, Y. (2014) DNA methylation modulates HRES1/p28 expression in B cells from patients with lupus. Autoimmunity, 47:265-271. PMID: 24117194; PMCID: PMC4034120

147. Talaber, G., Miklossy, G., Oaks, Z, Liu, Y, Tooze, S.A., Chudakov, D.M., Banki, K. and Perl. A (2014) HRES-1/Rab4 promotes the formation of LC3⁺ autophagosomes and the accumulation of mitochondria during autophagy. PLoS ONE, 9(1): e84392.

148. Caza, T., Oaks, Z and Perl, A. (2014) Interplay of infections, autoimmunity, and immunosuppression in systemic lupus erythematosus. Int. Rev. Immunol. 33(4):330-363.

149. Doherty, E, Oaks, Z. and Perl, A. (2014)系统性红斑狼疮患者淋巴细胞中n -乙酰半胱氨酸调节线粒体电子传递链复合物I活性增加. Antioxid. Redox Signal. 21: 56-65. PMID: 24673154;

150. Kato, H. and Perl, A. (2014) Mechanistic Target of Rapamycin Complex 1 Expands Th17 and IL-4⁺ CD4^-CD8^- Double-Negative T Cells and Contracts Regulatory T Cells in Systemic Lupus Erythematosus. J. Immunol. 192:4134-4144; PMID: 24683191. PMCID: PMC3995867.

151. Oaks Z and Perl A. TALDO1 (transaldolase 1). Atlas Genet Cytogenet Oncol Haematol. Feb 2014; 18(2).

152. Lai, Z-W, Marchena-Mendez, I. and Perl, A. (2015) Oxidative stress and Treg depletion in lupus patients with anti-phospholipid syndrome. Clin. Immunol. 158:148-152. PMID: 26366134; PMCID:PMC4464983

153. Perl, A. (2015) mTOR Activation is a Biomarker and Central Pathway to Autoimmune Disorders, Cancer, Obesity, and Aging. Ann. NY Acad. Sci. 1346:33-44. PMID: 25907074; PMCID: PMC4480196

154. Liu, Y., Yu, J., Oaks, Z.,  Marchena-Mendez, I., Francis, L., Bonilla, E., Aleksiejuk, P., Patel, J, Banki, K., Landas, S.K. and Perl, A. (2015)肝损伤与自身免疫和疾病活动性的生物标志物相关，并代表系统性红斑狼疮患者的器官系统受累. Clin. Immunol. 160:319-327. PMID: 26366134; PMCID:PMC4583603

155. Perl, A., Hanczko, R., Lai, Z-W, Oaks, Z., Kelly, R., Borsuk, R., Asara, J.M., and Phillips, P.E. (2015)综合代谢组学分析揭示了系统性红斑狼疮中n -乙酰半胱氨酸反应性犬尿氨酸积累:对雷帕霉素机制靶点激活的影响. Metabolomics. 11:1157-1174. PMID: 26366134; PMCID: PMC4559110

156. Joseph, N., Zhang-James, Y., Perl, A., and Faraone, S.V. (2015) Oxidative Stress and Attention Deficit Hyperactivity Disorder: A Meta-Analysis. J. Atten. Disord. 19:915-924. PMID: 24232168; PMCID: PMC5293138

157. Perl, A. (2016). Mechanistic Target of Rapamycin Pathway Activation in Rheumatic Diseases. Nat. Rev. Rheumatol. 12:169-182. PMID: 24232168; PMCID: PMC5314913

158. Klionsky, D.H...Perl, A... (2016) Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy. Autophagy. 12: 1-122. PMID: 24232168 PMCID:PMC4835977 [Available on 2017-01-21]

159. Oaks, Z., Winans, T, Caza, T., Fernandez, D., Liu, Y, Landas, S.K, Banki, K. and Perl, A. (2016)在狼疮易感小鼠中，肝脏线粒体功能障碍和抗磷脂抗体产生先于疾病发作，并对雷帕霉素有反应. Arthritis Rheumatol. (Featured In This Issue). 68(11):2728-2739. PMID: 27332042; PMCID:PMC5083168

160. Perl, Al. (2016) LINEing Up to Boost Interferon Production: Activation of Endogenous Retroviral DNA in Autoimmunity. Arthritis Rheumatol. Invited Editorial. 68:2568-2570. PMID: 27338170; PMCID: PMC5083194

161. Buskiewicz, I.A., Montgomery, T., Yasewicz, E.C., Huber, S.A., Murphy, M.P., Hartley, R.C., Kelly, R., Crow, M.K., Perl, A_, Budd, R.C. and Koenig, A. (2016) Reactive oxygen species induce virus-independent MAVS-oligomerization in systemic lupus erythematosus. Sci. Signal. Vol. 9, Issue 456, pp. ra115 DOI: 10.1126/scisignal.aaf1933. PMID: 27899525; PMCID: PMC5321043

162. Perl, A., Lai, Z,  Oaks, Z., Asara, A., Hanczko, R., Kelly, R., and Phillips, P. (2016).

Metabolome checkpoints of mTOR activation and clinical responsiveness in SLE. Lupus Sci. Med. (Suppl.1) A14-A15. http://dx.doi.org/10.1136/lupus-2016-000179.29

163. Oaks, Z, Winans, T, Huang, N, Banki, K. and Perl, A. (2016) Activation of the mechanistic target of rapamycin in SLE: Explosion of evidence in the last five years. Curr. Rheum. Rep. Dec;18(12):73. PMID.PMID: 27812954; DOI:10.1007/s11926-016-0622-8

164. Bonilla E, Shadakshari A, Perl A. (2016) Association of psoriasis and psoriatic arthritis with systemic lupus erythematosus. Rheumatol. Orthop. Med. http://oatext.com/pdf/ROM-1-105.pdf; DOI: 10.15761/ROM.1000105.

165. Doherty, E. and Perl, A. (2017) Measurement of Mitochondrial Mass by Flow Cytometry during Oxidative Stress. React. Oxyg. Species, 4 (10): 275-283. ISSN 2380-2367. PMID: 29806036; PMCID: PMC5964986

166. Perl, A. (2017) Metabolic control of immune system activation in rheumatic diseases. Arthritis Rheumatol. 69:2259-2270. PMID: 28841779 PMCID: PMC5711528 [Available on 2018-12-01]

167. Kato, H. and Perl, A. (2018) IL-21-mTOR轴通过抑制自噬来阻断系统性红斑狼疮患者调节性T细胞的分化和功能. Arthritis Rheumatol. 70(3):427-438. PMID: 29161463; PMCID: PMC5826851

168. Lai, Z, Kelly, R., Winans, T., Marchena, I., Shadakshari, A., Yu, J.,  Dawood, M., Garcia, R., Tily, H. Francis, L., Faraone, S.V .,  Phillips, P.E. and Perl, A. (2018) Sirolimus in patients with clinically active systemic lupus erythematosus resistant to, or intolerant of, conventional medications: a single-arm, open-label, phase 1/2 trial. Lancet, 391:1186-1196. PMID: 29551338;

PMCID: PMC5891154

169. Huang, N. and Perl, A. (2018) Metabolism as a target for modulation in autoimmune diseases. Trends Immunol. 39:562-576. PMID: 29739666;

170. Minchenberg SB, Chaparala G, Oaks Z, Banki K, and Perl A (2018) Systemic lupus erythematosus-myasthenia gravis overlap syndrome: Presentation and treatment depend on prior thymectomy. Clin. Immunol. 194:100-104. PMID: 30025818; PMC6089637.

171. Perl, A., Lai, Z, Kelly, R., Faraone, S.V., and Phillips, P.E. (2018) Sirolimus for systemic lupus erythematosus - Authors' reply. Lancet, 392:734. PMID: 30191826;

172. Zhi-Wei Lai, Ryan Kelly, Thomas Winans, Ivan Marchena, Ashwini Shadakshari, Julie Yu, Maha Dawood, Ricardo Garcia, Hajra Tily, Lisa Francis, Stephen V Faraone, Paul E Phillips和Andras Perl(2018)阻断雷帕霉素的机制靶点，通过抑制活动性SLE患者的促炎T细胞谱系特异性，可以快速持久地改善疾病活动性. Lupus Sci. Med. Aug 2018, 5 (Suppl 2) A13-A14; DOI: 10.1136/lupus-2018-lsm.26

173. Perl, A. (2018) mTOR-Dependent Autophagy Contributes to End-Organ Resistance and Serves as Target for Treatment in Autoimmune Disease. EBioMedicine, 36:12-13; PMID: 30262258; PMC6197622; DOI: 10.1016/j.ebiom.2018.09.033

174. Budd, R., Perl, A., Blanco, L., Kaplan, M. J., Buskiewicz, I., Fortner, K. (2018) Redox-driven type I interferon in SLE and its treatment with MitoQ. Lupus Sci. Med. 6 (Suppl. 1) A28-A29; http://dx.doi.org/10.1136/lupus-2019-lsm.38

175. Liu, E. and Perl, A. (2019) Pathogenesis and treatment of autoimmune rheumatic diseases. Curr. Opin. Rheum. 31: 307-315. PMID: 30920455; PMCID: PMC6447054  [Available on 2020-05-01]

176. Oaks, Z., Jimah. J., Grossman, C.C., Beckford, M., Kelly, R., Banerjee, S., Niland, B., Miklossy, G., Kuloglu, Z., Kansu, A., Lee, W., Szonyi, L., Banki, K. and Perl, A., (2020) Transaldolase haploinsufficiency in subjects with acetaminophen-induced liver failure. J. Inherit. Metab. Dis. 43: 496-506. PMID: 31769880

177. Godavarthy, A., Kelly, R, Jimah, J., Beckford, M., Caza, T., Fernandez, D.R., Huang, N., Duarte, M., Lewis, J., Fadel, H.J., Poeschla, E.M., Banki, K. and Perl, A., (2020) Lupus-associated endogenous retroviral LTR polymorphism and epigenetic imprinting promote HRES-1/Rab4 expression and mTOR activation. JCI Insight, 5: e134010. PMID:31805010

178. Wyman, B. and Perl, A. (2020) Metabolic pathways mediate pathogenesis and offer targets for treatment in rheumatic diseases. Curr. Opin. Rheum. 32:184-191. PMID:31895126

179. Greca, I., Ben Gabr, J., Perl, A., Bryant, S. and Zaccarini, D. (2020) Trauma Induced Calcium Pyrophosphate Deposition Disease of the Lumbar Spine. Case Rep. Rheumatol. http://doi.org/10.1155/2020/3218350; PMID: 32095306;

180. Fortner K.A., Blanco, L.P., Buskiewicz, I., Huang, N., Gibson, P.C., Cook, D.L., Yuen, P.S.T., Murphy, M.P., Perl, A, Kaplan,^, M.J., Budd, R.C (2020) Targeting Mitochondrial Oxidative Stress with MitoQ Reduces NET Formation and Kidney Disease in Lupus-Prone MRL-lpr Mice. Lupus Sci. Med. PMID: 32343673; PMCID: PMC7199895; doi: 10.1136/lupus-2020-000387

181. Dziamski, K., Sharmeen, S., Banki, K., and Perl, A. (2020) Nine-test panel has superior sensitivity to detect antiphospholipid antibody syndrome in patients with or without SLE. Clin. Immunol. In press. PMID: 32200114; PMCID: PMC7200285 (available on 2021-05-01); DOI: 10.1016/j.clim.2020.108388

182. Piranavan, P., Bhamra, M. and Perl, A. (2020). Metabolic targets for treatment of autoimmune diseases. Immunometabolomics, 2020; 2(2): e200012. doi: 10.20900/immunometab20200012. PMID: 32341806; PMCID: PMC7184931

183. Piranavan, P. and Perl, A. (2020). Management of cardiovascular disease in patients with systemic lupus erythematosus. Expert Opin. Pharmacother. 21:1617-1628. PMID: 32511034;

184. Ben Gabr, J., Liu, E., Mian, S., Pillittere, J., Bonilla, E., Banki, K., Perl, A (2020) emapalumab成功治疗1例新诊断成人发病斯蒂尔氏病患者继发性巨噬细胞激活综合征:病例报告及文献综述. Ann. Transl. Med. 2020 Jul;8(14):887. doi: 10.21037/atm-20-3127. PMID: 32793731; PMCID: PMC7396773.

185. Ben Gabr, J., Bilal, H., Mirchia, K. and Perl, A (2020) The Use of Eculizumab in Tacrolimus-Induced Thrombotic Microangiopathy. J. Investig. Med. High Impact Case Rep. 8:2324709620947266; PMID: 32757799; PMCID: PMC7412890

186. Ibrahim, H, Perl, A., Smith, D., Lewis, T., Kon, Z., Goldenberg, R., Yarta, K., Staniloae, C., Williams, M. (2020) Therapeutic blockade of inflammation in severe COVID-19 infection with intravenous N-acetylcysteine. Clin. Immunol. 219:108544. PMID: 32707089;

PMCID: PMC7374140.

187. Pillittere, J., Mian, S., Richardson, T.E., and Perl, A. (2020) Hydroxychloroquine-Induced Toxic Myopathy Causing Diaphragmatic Weakness and Lung Collapse Requiring Prolonged Mechanical Ventilation. J. Investig. Med. High Impact Case Rep. doi: 10.1177/2324709620950113; PMID: 32787461; PMCID: PMC7427040

188. Kato, H. and Perl, A. (2021) Double-Edged Sword: Interleukin-2 Promotes T regulatory Cell Differentiation but Expands Interleukin-13- and Interferon-γ-producing CD8⁺ T cells via STAT6-GATA-3 Axis in Systemic Lupus Erythematosus. Front. Immunol. PMID: 33763079;

189. Klionsky, D.H...Perl, A... (2021) Guidelines for the Use and Interpretation of Assays for Monitoring Autophagy (4^th edition). Autophagy. 12: 1-382. PMID: 33634751; PMCID:

190. Piranavan, P. and Perl, A. (2021) Improvement of renal and non-renal SLE outcome measures on sirolimus therapy - a 21-year follow-up study of 73 patients. Clin. Immunol. 229:108781. PMID: 34144197;

191. Geier, C. and Perl A. (2021). Therapeutic mTOR blockade in systemic autoimmunity: implications for antiviral immunity and extension of lifespan. Autoimmun. Rev. 20:102984. PMID: 34718162; PMCID: PMC8550885

192. Nasr, S, Khalil, S, Poiesz, B, Banki, K, Perl, A. (2021) Pfizer-BioNTech COVID‑19 RNA vaccination induces phosphatidylserine autoantibodies, cryoglobulinemia, and digital necrosis in a patient with pre-existing autoimmunity. Clin. Immunol. Commun. 1:1-3.

193. Patel, A. and Perl, A. (2022). Redox control of integrin-mediated hepatic inflammation in systemic autoimmunity. Antioxid. Redox Signal. 36: 367-388. PMID: 34036799

194. Levack, R.C., Newell, K.L., Cabrera-Martinez, B., Cox, J., Perl, A., Bastacky, S.I. and Winslow, G.M. (2022) Adenosine Receptor 2a Agonists Target Mouse CD11c+Tbet+ B cells in Infection and Autoimmunity. Nat. Commun. 13:452. PMID: 35064115

195. Zhaomin, M, Tan, Y, Tao, J, Li, L, Wang, Hui, Yu, F., Perl, A. and Zhao, M. (2022). Renal mTORC1 Activation is Associated with Disease Activity and Prognosis in Lupus Nephritis. Rheumatology. 61:3830-3840. PMID: 35040950

196. El-Dokla, A., Bonilla, E. and Perl, A. (2022) Recurrent brachial plexopathy as initial presentation of systemic lupus erythematosus: a case report and review of the literature. Lupus, 31:500-504. PMID: 35259024

197. Caza, T., Wijewardena, C. Al-Rabadi, L. and Perl, A. (2022). Cell Type-Specific Mechanistic Target of Rapamycin-Dependent Distortion of Autophagy Pathways in Lupus Nephritis. Transl. Res. 245: 55-81. PMID: 35288362

198. Anuforo, A, Sandhu, M., Yu, J. and Perl, A. (2022) Appraising SARS-CoV-2 infections after full mRNA COVID-19 vaccination in patients with systemic lupus erythematosus (SLE). Clin. Immunol. Commun. 2:54-56.

199. Brown, J., Abboud, G., Ma, L., Choi, S-C., Kanda, N., Zeumer-Spataro, L., Lee, J., Peng, W., Cagmat, J., Faludi, T., Mohamadzadeh, M., Garrett, T., Mandik-Nayak, L., Chervonsky, A., Perl, A., and Morel, L. (2022). Microbiota-mediated skewing of tryptophan catabolism modulates CD4⁺ T cells in lupus-prone mice. iScience, 25:104241. PMID: 35494242; PMCID: PMC9051618

200. Perl, A., Agmon-Levin, N., Crispín, J.C. and Jorgensen, T.N. (2022)系统性红斑狼疮诊断和治疗的新生物标志物:连接多组学和系统生物学之间的点. Editorial. Front. Immunol. 13:1009038. PMID: 36311710; PMCID: PMC9599399

201. Nasr, S. and Perl, A. (2022) Principles behind SLE treatment with N-acetylcysteine. Immunometabolism, 4:e00010. PMID: 36312742; PMCID: PMC9605192

202. Oaks, Z, Patel, A, Huang, N, Choudhary, G, Winans, T, Faludi, T, Krakko, D, Duarte, M, Lewis, J, Beckford, M, Blair, S, Kelly, R, Landas, SK, Middleton, FA, Asara, JM, Chung, SK, Fernandez, DR, Banki, K, and Perl, A. (2023) Cytosolic aldose metabolism contributes to progression from cirrhosis to hepatocarcinogenesis. Nat. Metab. 5:41-60. PMID: 36658399;

203. Grossman, C. E. and Perl, A. (2023)戊糖磷酸途径参与脂肪细胞分化:在脂肪形成阶段，转醛缩酶的表达被选择性上调. Submitted.