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Systemic Lupus Erythematosus: HELP
Articles from Ithaca
Based on 12 articles published since 2009

These are the 12 published articles about Lupus Erythematosus, Systemic that originated from Ithaca during 2009-2019.
+ Citations + Abstracts
1 Review Rho Kinases in Autoimmune Diseases. 2016

Pernis, Alessandra B / Ricker, Edd / Weng, Chien-Huan / Rozo, Cristina / Yi, Woelsung. ·Autoimmunity and Inflammation Program, Hospital for Special Surgery, New York, NY 10021; email: pernisa@hss.edu , RozoC@hss.edu , YiW@hss.edu. · Graduate Program in Immunology and Microbial Pathogenesis, Weill Cornell Graduate School of Medical Sciences, New York, NY 10065; email: edr2007@cornell.edu. · David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, NY 10021. · Department of Medicine, Weill Cornell Medical College, Cornell University, New York, NY 10021. · Graduate Program in Biochemistry Cell and Molecular Biology, Weill Cornell Graduate School of Medical Sciences, New York, NY 10065; email: chw2019@cornell.edu. ·Annu Rev Med · Pubmed #26768244.

ABSTRACT: The Rho kinases, or ROCKs, are a family of serine-threonine kinases that serve as key downstream effectors for Rho GTPases. The ROCKs are increasingly recognized as critical coordinators of a tissue response to injury due to their ability to modulate a wide range of biological processes. Dysregulated ROCK activity has been implicated in several human pathophysiological conditions ranging from cardiovascular and renal disorders to fibrotic diseases. In recent years, an important role for the ROCKs in the regulation of immune responses is also being uncovered. We provide an overview of the role of the ROCKs in immune cells and discuss studies that highlight the emerging involvement of this family of kinases in the pathogenesis of autoimmune diseases. Given the potential promise of the ROCKs as therapeutic targets, we also outline the approaches that could be employed to inhibit the ROCKs in autoimmune disorders.

2 Review Postoperative risk of venous thromboembolism in rheumatic disease patients. 2015

Wong, Lauren E / Bass, Anne R. ·Weill Cornell Medical College, 186 Joralemon Street, Brooklyn, NY, 11201, USA, law9044@med.cornell.edu. ·Curr Rheumatol Rep · Pubmed #25691333.

ABSTRACT: Both traditional and disease-related risk factors for venous thromboembolism (VTE) must be considered when assessing rheumatic disease patients preoperatively. While many studies suggest that patients with rheumatic diseases are at higher risk of VTE overall, studies in rheumatoid arthritis patients do not demonstrate an increased risk of postoperative VTE. Here, we review the literature on VTE risk in patients with rheumatoid arthritis, systemic lupus erythematosus, Behcet's disease, and vasculitis. The data suggest that disease activity is a driver of VTE risk. While rheumatoid arthritis patients undergoing elective arthroplasty are not at elevated VTE risk, patients with systemic lupus erythematosus and antiphospholipid antibody syndrome undergoing surgery have an elevated risk of postoperative VTE.

3 Review Renal disease in systemic lupus erythematosus with emphasis on classification of lupus glomerulonephritis: advances and implications. 2009

Seshan, Surya V / Jennette, J Charles. ·Department of Pathology and Laboratory Medicine,Weill Cornell Medical College, New York-Presbyterian Hospital, 525 E 68th Street, New York, NY 10065, USA. svs2002@med.cornell.edu ·Arch Pathol Lab Med · Pubmed #19195967.

ABSTRACT: CONTEXT: Systemic lupus erythematosus is an autoimmune disease with protean clinical and pathologic manifestations involving almost all organs in the body. There is a high incidence of renal involvement during the course of the disease, with varied renal pathologic lesions and diverse clinical features. A renal biopsy examined by routine light microscopy, immunofluorescence, and electron microscopy contributes toward diagnosis, prognostic information, and appropriate management. OBJECTIVES: (1) To review the clinical and various pathologic features of renal lesions in systemic lupus erythematosus patients. (2) To introduce the International Society of Nephrology and Renal Pathology Society Classification of Lupus Glomerulonephritis. DATA SOURCES: A literature review, illustrations with original artwork, and tabulation of clinical and pathologic data of cases obtained from the authors' renal biopsy files examined during the last 8 years were used. CONCLUSIONS: The International Society of Nephrology/ Renal Pathology Society-sponsored Classification of Lupus Glomerulonephritis proposes standardized definitions of the various pathologic findings, describes clinically relevant lesions, incorporates prognostic parameters, and recommends a uniform way of reporting the renal biopsy findings. Lupus glomerulonephritis is divided into 6 classes primarily based on the morphologic lesions, extent and severity of the involvement, immune complex deposition, and activity and chronicity. Special emphasis is laid on describing qualitative as well as quantitative morphologic data and to include the accompanying tubulointerstitial disease and different vascular lesions, which have prognostic and therapeutic significance. This classification is intended to facilitate a higher degree of reproducibility, resulting in better patient care and more effective future clinical and translational research. Renal biopsy findings in systemic lupus erythematosus add new and independent parameters of prognostic significance to established clinical and genetic factors.

4 Article A CD4 2019

Caielli, Simone / Veiga, Diogo Troggian / Balasubramanian, Preetha / Athale, Shruti / Domic, Bojana / Murat, Elise / Banchereau, Romain / Xu, Zhaohui / Chandra, Manjari / Chung, Cheng-Han / Walters, Lynnette / Baisch, Jeanine / Wright, Tracey / Punaro, Marilynn / Nassi, Lorien / Stewart, Katie / Fuller, Julie / Ucar, Duygu / Ueno, Hideki / Zhou, Joseph / Banchereau, Jacques / Pascual, Virginia. ·Baylor Institute for Immunology Research, Dallas, TX, USA. · Drukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA. · Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA. · The Jackson Laboratory for Genomic Medicine, Farmington, CT, USA. · Texas Scottish Rite Hospital for Children, Dallas, TX, USA. · Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA. · Mount Sinai School of Medicine, New York, NY, USA. · Pathologists Bio-Medical Laboratories, Lewisville, TX, USA. · Baylor Institute for Immunology Research, Dallas, TX, USA. vip2021@med.cornell.edu. · Drukier Institute for Children's Health, Weill Cornell Medicine, New York, NY, USA. vip2021@med.cornell.edu. · Department of Pediatrics, Weill Cornell Medicine, New York, NY, USA. vip2021@med.cornell.edu. · Texas Scottish Rite Hospital for Children, Dallas, TX, USA. vip2021@med.cornell.edu. ·Nat Med · Pubmed #30478422.

ABSTRACT: Understanding the mechanisms underlying autoantibody development will accelerate therapeutic target identification in autoimmune diseases such as systemic lupus erythematosus (SLE)

5 Article Serologic features of cohorts with variable genetic risk for systemic lupus erythematosus. 2018

Bhattacharya, Jyotsna / Pappas, Karalyn / Toz, Bahtiyar / Aranow, Cynthia / Mackay, Meggan / Gregersen, Peter K / Doumbo, Ogobara / Traore, Abdel Kader / Lesser, Martin L / McMahon, Maureen / Utset, Tammy / Silverman, Earl / Levy, Deborah / McCune, William J / Jolly, Meenakshi / Wallace, Daniel / Weisman, Michael / Romero-Diaz, Juanita / Diamond, Betty. ·The Feinstein Institute for Medical Research, Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases, 350 Community Dr, Manhasset, NY, 11030, USA. · Department of Statistical Science, Cornell University, Ithaca, NY, USA. · Department of Internal Medicine, Istanbul University, Istanbul, Turkey. · The Feinstein Institute for Medical Research, Center for Genomics and Human Genetics, Manhasset, NY, USA. · Malaria Research and Training Center, Bamako, Mali. · Deputy of the Department of Internal Medicine, University Hospital, Bamako, Mali. · The Feinstein Institute for Medical Research, Center of Biostatistics Unit Manhasset, Manhasset, NY, USA. · UCLA David Geffen School of Medicine, Los Angeles, CA, 90095, USA. · University of Chicago Medical Center, Chicago, IL, USA. · Hospital for Sick Children, University of Toronto, Toronto, ON M5G, 1X8, Canada. · University of Michigan, Ann Arbor, MI, 48109, USA. · Rush University Medical Center, Chicago, IL, 60612, USA. · Cedars Sinai Medical Center, Los Angeles, CA, 90048, USA. · Instituto Nacional de Ciencias Medicas y Nutrician Salvador Zubiran, Mexico City, Mexico. · The Feinstein Institute for Medical Research, Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases, 350 Community Dr, Manhasset, NY, 11030, USA. bdiamond@northwell.edu. ·Mol Med · Pubmed #30134810.

ABSTRACT: BACKGROUND: Systemic lupus erythematosus (SLE) is an autoimmune disease with genetic, hormonal, and environmental influences. In Western Europe and North America, individuals of West African descent have a 3-4 fold greater incidence of SLE than Caucasians. Paradoxically, West Africans in sub-Saharan Africa appear to have a low incidence of SLE, and some studies suggest a milder disease with less nephritis. In this study, we analyzed sera from African American female SLE patients and four other cohorts, one with SLE and others with varying degrees of risk for SLE in order to identify serologic factors that might correlate with risk of or protection against SLE. METHODS: Our cohorts included West African women with previous malaria infection assumed to be protected from development of SLE, clinically unaffected sisters of SLE patients with high risk of developing SLE, healthy African American women with intermediate risk, healthy Caucasian women with low risk of developing SLE, and women with a diagnosis of SLE. We developed a lupus risk index (LRI) based on titers of IgM and IgG anti-double stranded DNA antibodies and levels of C1q. RESULTS: The risk index was highest in SLE patients; second highest in unaffected sisters of SLE patients; third highest in healthy African-American women and lowest in healthy Caucasian women and malaria-exposed West African women. CONCLUSION: This risk index may be useful in early interventions to prevent SLE. In addition, it suggests new therapeutic approaches for the treatment of SLE.

6 Article Association between rs2294020 in X-linked CCDC22 and susceptibility to autoimmune diseases with focus on systemic lupus erythematosus. 2017

D'Amico, Fabio / Skarmoutsou, Evangelia / Lo, Lauren J / Granata, Mariagrazia / Trovato, Chiara / Rossi, Giulio A / Bellocchi, Chiara / Marchini, Maurizio / Scorza, Raffaella / Mazzarino, Maria Clorinda / Keinan, Alon. ·Department of Biomedical and Biotechnological Sciences, University of Catania, Via Androne 83, I-95124 Catania, Italy. Electronic address: f.damico@unict.it. · Department of Biomedical and Biotechnological Sciences, University of Catania, Via Androne 83, I-95124 Catania, Italy. · Department of Biological Statistics and Computational Biology, Cornell University, Ithaca, NY 14853, USA. · Referral Center for Systemic Autoimmune Diseases, University of Milan and Fondazione IRCCS Ospedale Maggiore Policlinico, Mangiagalli e Regina Elena, Via Pace 9, I-20122 Milan, Italy. ·Immunol Lett · Pubmed #27888057.

ABSTRACT: Autoimmune diseases often share common susceptibility genes. Most genetic variants associated with susceptibility to systemic lupus erythematosus are also associated with other autoimmune diseases. The X-linked variant rs2294020 is positioned in exon 7 of the CCDC22 gene. The encoded protein functions in the regulation of NF-κB, a master regulator in immune response. The aim of this study is to investigate whether the rs2294020 polymorphism may be a general susceptibility factor for autoimmunity. We evaluated case-control association between the occurrence of rs2294020 and different autoimmune diseases, including new data for systemic lupus erythematosus and previous genome-wide association studies (GWAS) (though most did not analyse the X chromosome) of psoriasis, celiac disease, Crohn's disease, ulcerative colitis, multiple sclerosis, vitiligo, type-1 diabetes, rheumatoid arthritis, and ankylosing spondylitis. Cases from patients affected by amyotrophic lateral sclerosis and type-2 diabetes were also included in the study. We detected nominal significant associations of rs2294020 with systemic lupus erythematosus (additive model test: p=0.01), vitiligo (p=0.016), psoriasis (p=0.038), and in only one of two studies of multiple sclerosis (p=0.03). Our results suggest that rs2294020 is associated with the risk of several autoimmune diseases in European populations, specifically with diseases that present themselves, among else, in the skin.

7 Article Correlation between Doppler parameters and renal cortical fibrosis in lupus nephritis: a preliminary observation. 2013

Gao, Jing / Chevalier, James / Auh, Yong Ho / Rubin, Jonathan M / Wang, Hui / Sun, Li-Na / Seshan, Surya / Min, Robert. ·Department of Radiology, New York-Presbyterian Hospital, Weill Cornell Medical College, New York, New York 10065, USA. jig2001@med.cornell.edu ·Ultrasound Med Biol · Pubmed #23245821.

ABSTRACT: To assess the relationship between renal Doppler parameters and renal cortical fibrosis in lupus nephritis (LN), we retrospectively reviewed 24 patients with LN underwent both renal color Doppler sonography and renal biopsy. The angle-corrected Doppler parameters, including peak systolic velocity (PSV), end diastolic velocity (EDV) and resistive index (RI) at the main and interlobar renal arteries were measured. The Doppler parameters and PSV and EDV ratios of the interlobar artery to main renal artery were compared with histopathologic analysis of the kidney biopsy specimen. On the basis of renal cortical fibrosis, the 24 cases of LN were divided into two groups: mild (6%-25%) renal cortex fibrosis (n = 13) and moderate (26%-50%) renal cortex fibrosis (n = 11). An independent-samples two tailed t test was used to statistically analyze the differences in PSV, EDV and RI between the two groups. Receiver operating characteristic was analyzed for assessing the accuracy of interlobar artery PSV and EDV in predicting moderate renal cortical fibrosis. In our result, both PSV and EDV in moderate renal cortex fibrosis were lower than that in mild renal cortex fibrosis. There were statistically significant differences in PSV and EDV at the interlobar artery, EDV and RI at the main renal artery, and PSV and EDV ratios of the interlobar artery to main renal artery between the two groups (all p < 0.05). The area under receiver operating characteristic curves of PSV and EDV for predicting >26% renal cortical fibrosis was 0.96 and 0.90, respectively. The optimal cutoff values for differentiating >26% renal cortical fibrosis from those <25% were PSV 30 cm/s (sensitivity = 0.92; specificity = 1) and EDV 13 cm/s (sensitivity = 0.77; specificity = 1). Therefore, the values of PSV and EDV at the interlobar artery can potentially be used as hemodynamic indicators of renal cortical fibrosis, which may non-invasively assist in monitoring the progression of renal cortical fibrosis in LN, especially in patients with contraindications to renal biopsy.

8 Article 17β-Estradiol (E-2) administration to male (NZB × SWR)F₁ mice results in increased Id(LN)F₁-reactive memory T-lymphocytes and accelerated glomerulonephritis. 2012

Feng, F / Silvin, C J / Fiore, N C / Stoll, M L / Price, K E / Shanley, P S / Silverstone, A E / Gavalchin, J. ·Department of Microbiology & Immunology, Cornell University, Ithaca, NY 14853, USA. ·Lupus · Pubmed #22065096.

ABSTRACT: While it has been shown that estradiol treatment accelerates the onset of lupus nephritis with autoantibody production and kidney damage in both male and female lupus-prone mice, the specific mechanism(s) involved are unknown. Our previous work has shown that alterations in Id(LN)F(1)-reactive T cells and Id(LN)F(1)+ antibodies correlated closely with the onset of autoimmune nephritis in female F(1) progeny of SWR and NZB (SNF(1)) mice, supporting a critical role for the Id(LN)F(1) idiotype in the development of disease. Since male SNF(1) mice normally do not develop nephritis, we tested whether administration of 17β-estradiol (E-2) to male SNF(1) mice would increase Id(LN)F(1) IgG levels and autoreactive T cells, and further, induce nephritis. We found that E-2-treated male SNF(1) mice developed nephritis with the same time course and mean survival as normal female SNF(1) mice. Moreover, it appeared that the mechanism involved increased serum Id(LN)F(1)(+)IgG and its deposition in kidney glomeruli, preceded by a striking twofold increase in T-lymphocytes expressing the memory phenotype (CD44(+)CD45RB(lo)) predominantly in the Id(LN)F(1)-reactive T-cell population. In addition, we noted that cells with this phenotype were increased in the nephritic kidneys of treated mice, suggesting a direct involvement of those cells in the renal pathology. E-2 treatment also induced increased numbers of pathogenic Id(LN)F(1)+ antibody-producing B cells and elevated presentation of pathogenic Id(LN)F(1)+ peptide. Taken together, these results suggest a mechanism of E-2-induced acceleration of autoimmune disease in lupus-prone mice may involve expansion of autoreactive idiotypic T and B-cell populations.

9 Article A proposed framework to standardize the neurocognitive assessment of patients with pediatric systemic lupus erythematosus. 2010

Ross, Gail S / Zelko, Frank / Klein-Gitelman, Marisa / Levy, Deborah M / Muscal, Eyal / Schanberg, Laura E / Anthony, Kelly / Brunner, Hermine I / Anonymous3970664. ·Weill-Cornell Medical College, New York, New York 10021, USA. gsross@med.cornell.edu ·Arthritis Care Res (Hoboken) · Pubmed #20589693.

ABSTRACT: OBJECTIVE: To develop and propose a standardized battery of neuropsychological tests for the assessment of cognitive functioning of children and adolescents with pediatric systemic lupus erythematosus (SLE). METHODS: A committee of health care professionals involved in the assessment of pediatric SLE patients reviewed the literature to identify cognitive domains most commonly affected in pediatric SLE and in adult SLE. They then reviewed the standardized tests available for children and adolescents that assess the cognitive domains identified. Through a structured consensus formation process, the committee considered the psychometric characteristics and durations of the tests. RESULTS: A test battery was developed that appears suitable to provide a comprehensive assessment of cognitive domains commonly affected by pediatric SLE within a 2.5-hour period. CONCLUSION: It is hoped that the consistent use of this reliable and efficient battery increases the practicality of routine evaluations in pediatric SLE, enabling between-cohort comparisons and facilitating the longitudinal assessment of individual patients over time.

10 Article The induction of the lupus phenotype by estrogen is via an estrogen receptor-alpha-dependent pathway. 2010

Feng, Feng / Nyland, Jennifer / Banyai, Michelle / Tatum, Arthur / Silverstone, Allen E / Gavalchin, Jerrie. ·Department of Microbiology & Immunology, Cornell University, Ithaca, NY 14853, USA. ·Clin Immunol · Pubmed #19926524.

ABSTRACT: In order to investigate the roles of ER subtypes in the estrogen-induced lupus phenotype, ERalpha-deficient (ERalpha(-/-)) and wild-type mice (WT) were injected monthly with estradiol (E-2) starting at 8 weeks. In WT mice, E-2 treatment induced a lupus phenotype, with accelerated death and increased kidney damage, as well as Th2-type serum cytokine and autoantibody production. In contrast, only minimal changes were observed in ERalpha(-/-) mice after E-2 treatment. In a separate study, we found that in immune cells of autoimmune-prone SNF(1) and non-autoimmune DBF(1) mice, both ERalpha and ERbeta were differentially expressed and modulated by E-2. In SNF(1) mice, there were more CD4(+) and CD8(+) T cells constitutively expressing ERalpha, and the percentages of ERalpha+ dendritic cells and macrophages were increased after E-2 exposure compared to DBF(1) mice. Taken together, these observations strongly suggest a role for ERalpha in E-2-induced development of the lupus phenotype.

11 Article The phenotypic profile of dermatomyositis and lupus erythematosus: a comparative analysis. 2010

Magro, Cynthia M / Segal, Jeremy P / Crowson, A Neil / Chadwick, Paul. ·Department of Pathology, New York Presbyterian Hospital-Weill Cornell Medical Center, New York, NY 10044, USA. cym2003@med.cornell.edu ·J Cutan Pathol · Pubmed #19891658.

ABSTRACT: BACKGROUND: The mechanisms which regulate cutaneous inflammation in the setting of collagen vascular disease have been a topic of recent interest; emphasis has been placed on type I interferon-associated recruitment of CXCR3+ lymphocytes in dermatomyositis (DM). METHODS: On a total of 42 biopsies from patients with DM, systemic lupus erythematosus (SLE), discoid lupus erythematosus (DLE) and subacute cutaneous lupus erythematosus (SCLE) comprehensive phenotypic studies were performed to explore the practical value of phenotypic analysis in the subclassification of lesions of collagen vascular disease. RESULTS: The infiltrate in DM was of mild intensity compared to lupus erythematosus (LE). The dominant mononuclear cell in DM exhibited a CD4/CXCR3-positive phenotype while biopsies of SLE typically showed a dearth of CXCR3-positive cells. CD8 and CD20 lymphocytes were greatest in SLE and DLE, respectively. CD123 plasmacytoid dendritic cells, seen in most cases, were most frequent in cases of SCLE; CD83 expression was minimal. Endothelial MXA expression was a characteristic feature of DM. CD123 and MXA expression within inflammatory cells and keratinocytes was most conspicuous in areas of interface injury. Cutaneous lymphocyte antigen (CLA) expression was diminished in the dermal infiltrate in most cases of DM and LE. T regulatory cells never exceeded 15% of the infiltrate and were the least in the setting of DM and LE. CONCLUSIONS: An interferon-alpha-inducible cytokine milieu is common in SLE, DLE, SCLE and DM. In addition, there are phenotypic differences as alluded to above that may be of some practical value in separating these distinctive subsets. Features not previously emphasized such as MXA endothelial cell staining in DM and the lack of staining for CD83 and CLA in lesions of collagen vascular disease may be of diagnostic value.

12 Article High prevalence of subclinical cardiovascular abnormalities in patients with systemic lupus erythematosus in spite of a very low clinical damage index. 2009

Palmieri, V / Migliaresi, P / Orefice, M / Lupo, T / Di Minno, M N D / Valentini, G / Celentano, A. ·Unit of Cardiology, Ospedale dei Pellegrini, ASL Napoli 1, Naples, Italy. vpalmier@med.cornell.edu ·Nutr Metab Cardiovasc Dis · Pubmed #19157818.

ABSTRACT: BACKGROUND AND AIM: To evaluate the prevalence of subclinical cardiovascular (CV) abnormalities in systemic lupus erythematosus (SLE) stratified according to SLE-related organ damage using the Systemic Lupus International Collaborating Clinics (SLICC) damage index. METHODS AND RESULTS: We selected SLE patients without clinically overt CV events (n=45, 56% with SLICC=0, 44% with SLICC=1-4). CV evaluation was performed using cardiac and vascular echo-Doppler techniques. Post-ischemic flow-mediated dilation (FMD) over nitroglycerine-mediated dilation (NMD) of the brachial artery <0.70 defined endothelial dysfunction. The prevalence of preclinical CV abnormalities (CVAbn, including at least one of the following-carotid atherosclerosis, left ventricular (LV) hypertrophy, low arterial compliance, LV wall motion abnormalities, aortic regurgitation, FMD/NMD<0.70)-was 64% (16/25) in patients with SLICC=0 and 80% (16/20) in those with SLICC>0 (p=not significant (NS)). In particular, the prevalence of carotid atherosclerosis (28% vs. 16%), of LV hypertrophy (12% vs. 6%) and of LV wall motion abnormalities (15% vs. 12%), of low global arterial compliance (18% vs. 10%), prevalence of aortic regurgitation (30% vs. 18%) and/or aortic valve fibrosclerosis (10% vs. 8%), FMD<10% (14+/-5% vs. 14%+/-6) and prevalence of FMD/NMD<0.70 (53% vs. 52%) were comparable in SLE patients with SLICC>0 and in those with SLICC=0 (all p=NS). Of the SLE patients without carotid atherosclerosis, LV hypertrophy, low arterial compliance, LV wall motion abnormalities and aortic regurgitation (n=17), endothelial dysfunction was detected in 50% of those with SLICC=0 (6/12) and in 40% of those with SLICC>0 (2/5, p=NS). CONCLUSIONS: SLE patients with SLICC=0 often have an elevated CV risk profile due to subclinical manifestations of CV disease detectable by cardiac and vascular echo-Doppler evaluations.