Die Bedeutung einer unvollständigen Beseitigung apoptotischer Zellen für Ätiologie und Pathogenese des SLE

摘要: Systemic lupus erythematosus (SLE) is a complex prototypic autoimmune disease that based on genetic factors (complement deficiencies) and influenced by gender (female), environment (infections UV irradiation), as well random events (somatic mutations). The course of the genes (e.g. FcgammaRIIA) behaviour (sun-exposure). Inefficient clearance dying cells subsequent accumulation apoptotic cell remnants an intrinsic defect causing permanent presence cellular debris responsible for initiation autoimmunity. We favour hypothesis post-apoptotic accumulates in germinal centres, activates complement, serves survival signal B-cells had stochastically become autoreactive process somatic hypermutation (etiology). In autoantibodies against or adaptor molecules (SNEC) causes immune formation their pathological elimination, maintaining auto-inflammation. SLE-type autoimmunity addresses nucleic acid-containing antigens (viromimetica). Autoantibody-protein-nucleic-acid complexes are likely to be mistaken opsonised viruses. As consequence, system responds with production type-I interferons, hallmark SLE (pathogenesis). conclude pathogenicity strongly increased if autoantigens accessible formed, which may considered binary pyrogen formed from less pro-inflammatory components. accessibility cognate related impaired delayed cells.