Complement activation plays important roles in innate immunity. However, excessive or unregulated activation of complement can injure host tissues, not only causing local injuries but also systemic reactions. Autoimmune diseases such as rheumatoid arthritis, lupus nephritis and Guillain-Barre syndrome are among the pathological situations caused by aberrant activation of the host immune system and complement activation plays important roles to develop and/or augment these diseases.
Recent therapeutic approaches in autoimmune disease have involved biological response modifiers such as anti-TNF, anti- TNF receptor and anti-IL6 agents, in addition to traditional therapies such as corticosteroid, methotrexate, azathioprine, mizoribine and cyclophosphamide in collagen diseases. These new biological reagents have shown promise but sometimes cause severe side effects or complications, including interstitial pneumonia and predispose to other infections such as tuberculosis. New strategies may therefore be required. As an alternative therapeutic approach, anti-complement agents might become a treatment of choice to control autoimmune diseases.
This mini-review focuses on recent knowledge of the role of complement activation in human collagen diseases and the other autoimmune diseases, including relevant animal models, and discusses the possibility of using anti-complement therapies. Regulation of the complement system might be a new approach to be considered as an alternative therapeutic strategy.
Keywords: Anaphylatoxin, autoimmune diseases, complement, complement 3a receptor, membrane complement regulator, systemic lupus erythematosus, therapeutic strategy, innate immunity, unregulated, plasma, post-ischemic diseases, brain stroke, ischemic colitis, inflammatory diseases, lupus erythematosus, collagen disease, rheumatoid arthritis, cyclophosphamide, Mycophenolate mofetil, tacrolimus hydrate, immune-suppressive agents, myasthenia gravis, idiopathic thrombocytopenic purpura, bullous pemphigus, plasma exchange, refractory Crohn's disease, tumor necrosis factor, lymphocyte-targeted, granulomatosis, hemolytic anemia, infertility, carcinogenesis, hepatitis, scleroderma, Listeria meningitis, Streptococcus pneumonia, Enteroviral meningoencephalitis, hydrolysis, T cell, phagocytosis, debris, organisms, lectin pathway, anaphylatoxin activity, neutralizing antibodies, paroxysmal nocturnal hemoglobinuria, T lymphocytes, necrotic cells, myeloid, glomerular injuries, glomerulonephritis, apoptotic, cell death, Hypocomplementemia, sclerosis, cerebrospinal fluid, alopecia areata, renal biopsies, thyroiditis, insulin, islet cells, cross-sectional study, polymorphisms, Stool, Cobra venom, hyperthyroidism, Phosphorylation
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