title: Autoimmunity to protective molecules: is it the perpetuum mobile (vicious cycle) of autoimmune rheumatic diseases?
abstract: Apoptotic defects and impaired clearance of cellular debris are considered key events in the development of autoimmunity, as they can contribute to autoantigen overload and might be involved in the initiation of an autoimmune response. The C1q protein and mannose-binding lectin are activators of the complement system. The pentraxins are a group of highly conserved proteins including the short pentraxins, C-reactive protein and serum amyloid P, and the long pentraxin family member, pentraxin 3, all of which are involved in innate immunity and in acute-phase responses. In addition to their role in innate immunity and inflammation, each of these proteins participates in the removal of damaged and apoptotic cells. In this article, we discuss the clinical significance of different levels of these proteins, their role in the induction of or protection against autoimmunity, and the presence of specific autoantibodies against them in various autoimmune diseases.
authors.affiliation: Department of Medicine B and the Center for Autoimmune Diseases, Chaim Sheba Medical Center, Tel-Hashomer, and Sackler Faculty of Medicine, Tel-Aviv University, Israel.
authors.forename: Martine Szyper
authors.initials: MS
authors.lastname: Kravitz
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Shoenfeld
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology* / Q000502:physiology; D001327:Autoimmune Diseases / Q000276:immunology* / Q000503:physiopathology; D015551:Autoimmunity / Q000276:immunology; D015922:Complement C1q / Q000276:immunology; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal; D012216:Rheumatic Diseases / Q000276:immunology* / Q000503:physiopathology
chemical_list: D015922:Complement C1q