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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Immunology
Импакт фактор: 1.352 5-летний Импакт фактор: 3.347 SJR: 1.022 SNIP: 0.55 CiteScore™: 2.19

ISSN Печать: 1040-8401
ISSN Онлайн: 2162-6472

Выпуски:
Том 39, 2019 Том 38, 2018 Том 37, 2017 Том 36, 2016 Том 35, 2015 Том 34, 2014 Том 33, 2013 Том 32, 2012 Том 31, 2011 Том 30, 2010 Том 29, 2009 Том 28, 2008 Том 27, 2007 Том 26, 2006 Том 25, 2005 Том 24, 2004 Том 23, 2003 Том 22, 2002 Том 21, 2001 Том 20, 2000 Том 19, 1999 Том 18, 1998 Том 17, 1997 Том 16, 1996 Том 15, 1995 Том 14, 1994

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v25.i2.30
pages 123-140

T- and B-Cell Abnormalities in Systemic Lupus Erythematosus

Gyorgy Nagy
Section of Rheumatology, Departments of Medicine, Microbiology and Immunology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, NY 13210
Agnes Koncz
Section of Rheumatology, Departments of Medicine, Microbiology and Immunology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, NY 13210
Andras Perl
Section of Rheumatology, Departments of Medicine, Microbiology and Immunology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, NY 13210

Краткое описание

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by the production of antinuclear autoantibodies and clinical involvement in multiple organ systems. T cells from patients with SLE have been shown to be activated in vivo and provide help to autoreactive B cells. Abnormal expression of key signaling molecules, defective signal transduction pathways, and permanent mitochondrial dysfunction—associated with a significantly increased mitochondrial mass—appear to be the axis of T-lymphocyte dysfunction. Lupus T cells exhibit persistent mitochondrial hyperpolarization (MHP), cytoplasmic alkalinization, increased ROI production, and ATP depletion that mediate enhanced spontaneous and diminished activation-induced apoptosis and sensitize lupus T cells to necrosis. Necrotic, but not apoptotic, cell lysates activate dendritic cells and may account for increased interferon-α production, inflammation, and antinuclear antibody production. Recent data indicate that B cells are not merely the passive producers of autoantibodies, but also play a central role in autoimmunity via nonconventional mechanisms, including autoantigen presentation and modulation of other immune cells. This article reviews recent advancements in the understanding of the molecular mechanisms involved in the pathogenesis of lupus autoimmunity and highlights the development of novel therapies in SLE.


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