作者: E. L. Nasonov
DOI: 10.14412/1996-7012-2014-4-4-13
关键词: Immunology 、 Immune system 、 Belimumab 、 Germinal center 、 Naive B cell 、 Medicine 、 Cytokine 、 B-cell activating factor 、 Acquired immune system 、 B cell
摘要: Systemic lupus erythematosus (SLE) is a multifactorial disease caused by complex interactions between the genetic and environmental factors underlying various innate adaptive immunity disorders, including cytokine hyperproduction, abnormal B cell activation, impaired intracellular T-cell signaling, defective apoptotic necrotic clearance. A broad spectrum of disorders associated with susceptibility to and/or its definite variants has been identified. Our knowledge concerning mechanisms polyclonal activation in SLE advanced substantially. Various defects T cells regulating immune response have detected. The development genetic, epigenomic, transcriptomic, proteomic technologies could identify group pathogenetically relevant cytokines, BLyS (the B-lymphocyte stimulator most important component cytokine-mediated regulation function, proliferation, differentiation), interleukin (IL) 6, 17, 18, type 1 interferon, tumor necrosis factor- α , which are involved visceral inflammation damage. Large-scale clinical trials different medications, primarily biological agents (BA), were conducted patients SLE. Rituximab (RTM) first BA be used treat this disease. Despite official registration for therapy SLE, RTM included EULAR, ACR, Russia's Association Rheumatologists guidelines treatment. Belimumab, fully human recombinant IgG1λ monoclonal antibody, specially designed prevents interaction pBLyS receptors autoreactive transitional naive cells, giving rise suppression hyperresponsiveness, autoantibody synthesis particular. In addition, block may cause decreased survival germinal centers lymphoid organs, differentiation memory into autoantibody-producing proinflammatory cytokines (IL-21, IL-17, others) that play an role immunopathogenesis moderate efficacy, belimumab will able improve pharmacotherapy