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pathogenesis lupus

Jan Klocke, Katharina Kopetschke, Anna-Sophie Grießbach, Valerie Langhans, Jens Y Humrich, Robert Biesen, Duska Dragun, Andreas Radbruch, Gerd-Rüdiger Burmester, Gabriela Riemekasten, Philipp Enghard
Renal infiltration of inflammatory cells contributes to the pathogenesis of Lupus nephritis (LN). Current knowledge on the recruitment mechanisms relies mainly on findings in rodent models. Here, we assess various chemokine pathways in human LN by comparing urinary chemokine concentrations (in 25 patients with acute LN and in 78 lupus patients without active LN) with the expression of corresponding chemokine receptors on urinary leukocytes (in ten acute LN patients). Nine urinary chemokines were significantly elevated in LN patients and correlated with renal disease activity and urinary cell counts; however, their concentrations displayed considerable interindividual heterogeneity...
October 18, 2016: European Journal of Immunology
Gangduo Wang, Silvia S Pierangeli, Rohan Willis, Emilio B Gonzalez, Michelle Petri, M Firoze Khan
Even though systemic lupus erythematosus (SLE) is associated with high morbidity and mortality rates among young and middle-aged women, the molecular mechanisms of disease pathogenesis are not fully understood. Previous studies from our laboratory suggested an association between oxidative stress and SLE disease activity (SLEDAI). To further assess the role of reactive oxygen species (ROS) in SLE, we examined the contribution of lipid-derived reactive aldehydes (LDRAs)-specific immune complexes in SLE. Sera from 60 SLE patients with varying SLEDAI and 32 age- and gender- matched healthy controls were analyzed for oxidative stress and related markers...
2016: PloS One
Masayuki Mizui, George C Tsokos
Recent extensive research on interleukin-2 (IL-2)/IL-2 receptor (IL-2R) biology has revealed its critical role in the regulation of immune tolerance by influencing regulatory T (Treg) cell functions and survival. Since in vivo low-dose IL-2 administration in humans has been confirmed to be safe and effective in expanding Treg, it is likely that it may be considered for the treatment of several autoimmune diseases including systemic lupus erythematousus (SLE). A recent clinical trial demonstrated the safety and efficacy of low-dose IL-2 treatment on SLE...
November 2016: Current Rheumatology Reports
Ki-Sung Kwon, Hye-Young Cho, Yeun-Jun Chung
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organ systems. Although the etiology of SLE remains unclear, it is widely accepted that genetic factors could be involved in its pathogenesis. A number of genome-wide association studies (GWASs) have identified novel single-nucleotide polymorphisms (SNPs) associated with the risk of SLE in diverse populations. However, not all the SNP candidates identified from non-Asian populations have been validated in Koreans. In this study, we aimed to replicate the SNPs that were recently discovered in the GWAS; these SNPs have not been validated in Koreans or have only been replicated in Koreans with an insufficient sample size to conclude any association...
September 2016: Genomics & Informatics
Robert W Hoffman, Joan T Merrill, Marta M E Alarcón-Riquelme, Michelle Petri, Ernst R Dow, Eric Nantz, Laura K Nisenbaum, Krista M Schroeder, Wendy J Komocsar, Narayanan B Perumal, Matthew D Linnik, David C Airey, Yushi Liu, Guilherme V Rocha, Richard E Higgs
OBJECTIVE: Systemic lupus erythematosus (SLE) has substantial unmet medical need and its pathogenesis is incompletely understood. This study characterized baseline gene expression and pharmacodynamic (PD)-induced changes in whole blood gene expression from two phase III, 52-week (W), randomized, placebo-controlled, double-blind studies of 1,760 SLE patients treated with the B cell activating factor (BAFF)-blocking IgG4 monoclonal antibody, tabalumab. METHODS: Patient samples were obtained from ILLUMINATE-1 and -2 while control samples were from healthy donors...
October 9, 2016: Arthritis & Rheumatology
N Nikitakis, W Papaioannou, L I Sakkas, E Kousvelari
To date there is a major effort in deciphering the role of complex microbial communities, especially the oral and gut microbiomes, in the pathogenesis of various diseases. Increasing evidence indicates a key role for the oral microbiome in autoimmune diseases. In this review article, we discuss links of the oral microbiota to a group of autoimmune diseases, i.e., Sjögren's syndrome (SS), systemic lupus erythematosus (SLE), Crohn's disease (CD), and rheumatoid arthritis (RA). We particularly focus on factors that affect the balance between the immune system and the composition of microbiota leading to dysbiosis, loss of tolerance and subsequent autoimmune disease progression and maintenance...
October 7, 2016: Oral Diseases
Pietro Enea Lazzerini, Pier Leopoldo Capecchi, Giacomo Maria Guidelli, Enrico Selvi, Maurizio Acampa, Franco Laghi-Pasini
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease primarily affecting synovial joints and is characterized by persistent high-grade systemic inflammation. Proinflammatory cytokines, particularly interleukin-6 (IL-6), are of crucial importance in the pathogenesis of the disease, driving both joint inflammation and extra-articular comorbidities. Tocilizumab, a humanized IL-6 receptor-inhibiting monoclonal antibody, has been the first, and, to date, the only, IL-6 inhibitor approved for the treatment of RA...
2016: Drug Design, Development and Therapy
Seung-Chul Choi, Anton A Titov, Ramya Sivakumar, Wei Li, Laurence Morel
Cellular metabolism represents a newly identified checkpoint of effector functions in the immune system. A solid body of work has characterized the metabolic requirements of normal T cells during activation and differentiation into polarized effector subsets. Similar studies have been initiated to characterize the metabolic requirements for B cells and myeloid cells. Only a few studies though have characterized the metabolism of immune cells in the context of autoimmune diseases. Here, we review what is known on the altered metabolic patterns of CD4(+) T cells, B cells, and myeloid cells in lupus patients and lupus-prone mice and how they contribute to lupus pathogenesis...
November 2016: Current Rheumatology Reports
Sophia Giang, Antonio La Cava
T regulatory cells (Tregs) represent a phenotypically and functionally heterogeneous group of lymphocytes that exert immunosuppressive activities on effector immune responses. Tregs play a key role in maintaining immune tolerance and homeostasis through diverse mechanisms which involve interactions with components of both the innate and adaptive immune systems. As in many autoimmune diseases, Tregs have been proposed to play a relevant role in the pathogenesis of systemic lupus erythematosus (SLE), an autoimmune disease characterized by a progressive breakdown of tolerance to self-antigens and the presence of concomitant hyperactive immune responses...
November 2016: Current Rheumatology Reports
Tian Qian, Yan Chen, Xiaowei Shi, Jian Li, Fei Hao, Dongmei Zhang
CCAAT/enhancer-binding protein β (C/EBP β) has important roles in numerous signaling pathways. The expression of the majority of regulators and target gene products of C/EBP β, including tumor necrosis factor α-induced protein 3 (TNFAIP3) and TNFAIP3-interacting protein 1 (TNIP1), are upregulated in patients with systemic lupus erythematosus (SLE). The aim of the present study was to investigate whether C/EBP β expression is associated with SLE pathogenesis and correlates with TNIP1 and TNFAIP3 expression...
October 2016: Experimental and Therapeutic Medicine
Magdalena Janina Laskaj, Anne Troldborg, Ellen-Margrethe Hauge, Shervin Bahrami, Kristian Stengaard-Pedersen
OBJECTIVES: Human Endogenous Retroviruses (HERVs) are remnants of past retroviral infections in the human genome and have been implicated in different aspects of human biology. The aim of this study was to identify HERVs which are associated with the pathogenesis of Rheumatoid diseases represented by Systemic Lupus Erythematosus (SLE). METHODS: The study subjects included 45 female patients with SLE and 50 geographically and age matched healthy. Real-time RT-PCR analysis was used to examine the transcription levels of 11 genes with coding capacity for complete envelope protein in these individuals...
October 1, 2016: Arthritis & Rheumatology
Karl J Lackner, Nadine Müller-Calleja
We appreciate Dr Pengo's comments on our Forum article regarding the pathogenesis of the antiphospholipid syndrome (APS) [1, 2]. Perhaps, we should point out that our goal was a plea for an unbiased approach to APS. What we call the "dogma", i.e. the focus on β2-glycoprotein I (β2GPI) as the major if not exclusive culprit antigen in APS, has obviously narrowed the approach to APS research. We agree with Pengo that lupus anticoagulant (LA) is the subgroup of antiphospholipid antibodies (aPL) with the strongest association to clinical events, and that so called triple aPL positive persons are at an increased risk compared to single or double positive persons...
October 2, 2016: Journal of Thrombosis and Haemostasis: JTH
Shi-Yang Guan, Rui-Xue Leng, Muhammad Imran Khan, Humera Qureshi, Xiang-Pei Li, Dong-Qing Ye, Hai-Feng Pan
Autoimmune diseases contain a large number of pathologies characterized by various factors that contribute to a breakdown in self-tolerance. Cytokine-mediated immunity plays an essential role in the pathogenesis of varieties of autoimmune diseases. Recent studies reveal that interleukin-35 (IL-35), a newly identified cytokine of IL-12 family, is implicated in the pathogenesis of autoimmune diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), systemic sclerosis (SSc), etc. In this review, we will discuss the biological features of IL-35 and summarize recent advances in the role of IL-35 in the development and pathogenesis of autoimmune diseases; the discoveries gained from these findings might translate into future therapies for these diseases...
October 1, 2016: Inflammation
P Delfani, G Sturfelt, B Gullstrand, A Carlsson, M Kassandra, C A K Borrebaeck, A A Bengtsson, C Wingren
Systemic lupus erythematosus (SLE) is a severe chronic inflammatory autoimmune connective tissue disease. Despite major efforts, SLE remains a poorly understood disease with unpredictable course, unknown etiology and complex pathogenesis. Apoptosis combined with deficiency in clearing apoptotic cells is an important etiopathogenic event in SLE, which could contribute to the increased load of potential autoantigen(s); however, the lack of disease-specific protein signatures deciphering SLE and the underlying biological processes is striking and represents a key limitation...
September 30, 2016: Lupus
Taro Iwamoto, Timothy B Niewold
Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease characterized by immune complex formation with multi-organ manifestations. Lupus nephritis (LN) is one of the most severe types of organ damage in SLE, and it clearly contributes to increased morbidity and mortality due to SLE. LN occurs more frequently and is more severe in non-European ancestral backgrounds, although the cause of this disparity remains largely unknown. Genetic factors play an important role in the pathogenesis of SLE...
September 28, 2016: Clinical Immunology: the Official Journal of the Clinical Immunology Society
Shu-Hui Chen, Qiao-Li Lv, Lei Hu, Ming-Jing Peng, Gui-Hua Wang, Bao Sun
Although lupus is, by definition, associated with genetic and immunological factors, its molecular mechanisms remain unclear. The up-to-date research findings point out that various genetic and epigenetic factors, especially gene-specific and site-specific methylation, are believed to contribute to the initiation and development of systemic lupus erythematosus (SLE). This review presents and summarizes the association between abnormal DNA methylation of immune-related cells and lupus-like diseases, as well as the possible mechanisms of immune disorder caused by DNA methylation, aiming at a better understanding of the roles of aberrant DNA methylation in the initiation and development of certain forms of lupus and providing a new insight into promising therapeutic regimens in lupus-like diseases...
September 30, 2016: Clinical and Experimental Immunology
Ye Shu, Qinghua Hu, Hai Long, Christopher Chang, Qianjin Lu, Rong Xiao
Autoimmune diseases are characterized by aberrant immune responses against healthy cells and tissues. However, the exact mechanisms underlying the development of these conditions remain unknown. CD4+CD25+ regulatory T cells (Tregs) are a subset of mature T cells which have an important role in maintaining immune homeostasis and preventing autoimmune diseases. Forkhead box p3 (Foxp3), a member of the fork head transcription factor family, is recognized as a marker of CD4+CD25+ Tregs. The decreased number and/or function of CD4+CD25+ Tregs in peripheral blood and related tissues has been demonstrated in systemic lupus erythematosus, systemic sclerosis, and other autoimmune diseases, which are at least partially regulated by epigenetic mechanisms...
September 29, 2016: Clinical Reviews in Allergy & Immunology
J K Presto, E Z Hejazi, V P Werth
Cutaneous lupus erythematosus (CLE) is an autoimmune skin disease occurring in association with or without systemic lupus erythematosus (SLE). Although antimalarials are widely used as the first-line systemic agent, refractory cases may benefit from additional immunomodulators, immunosuppressives, and biologics. An interest in biological therapies for CLE has emerged in recent years due to novel insight into the pathogenesis of CLE. These targets include B cells, T cells, and cytokines that are involved in immune system pathways...
September 29, 2016: Lupus
Daniel Peckham, Thomas Scambler, Sinisa Savic, Michael F McDermott
Immune-mediated autoinflammatory diseases are occupying an increasingly prominent position among the pantheon of debilitating conditions that afflict mankind. This review focuses on some of the key developments which have occurred since the original description of autoinflammatory disease in 1999, and focuses on underlying mechanisms that trigger autoinflammation. The monogenic autoinflammatory disease range has expanded considerably during that time, and now includes a broad spectrum of disorders, including relatively common conditions such as cystic fibrosis and subsets of systemic lupus erythematosus...
September 29, 2016: Journal of Pathology
Stavros Giaglis, Sinuhe Hahn, Paul Hasler
Neutrophil extracellular trap (NET) formation represents a form of cell death distinct from apoptosis or necrosis, by which invading pathogens are simultaneously entangled and potentially eliminated. Increased NET formation is observed in systemic lupus erythematosus (SLE), rheumatoid arthritis, antineutrophil cytoplasmic antibody-associated small vessel vasculitis, antiphospholipid antibody syndrome (APS), and psoriasis. NETs contribute to the pathogenesis of autoimmunity by exposing cryptic autoepitopes, which may facilitate the generation of autoantibodies, induce the production of interferons, and activate the complement cascade...
2016: Frontiers in Pediatrics
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