title: Autoantibodies against protective molecules--C1q, C-reactive protein, serum amyloid P, mannose-binding lectin, and apolipoprotein A1: prevalence in systemic lupus erythematosus.
abstract: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of several autoantibodies. Among the multiple factors involved in SLE development, apoptotic defects and impaired clearance of cellular debris have gained considerable interest, as they contribute to autoantigen overload. Several molecules of the innate immunity, also participate in the removal of damaged and apoptotic cells. Among them are C1q, C-reactive protein (CRP), serum amyloid P protein (SAP), mannose-binding lectin (MBL), and apolipoprotein A1 (APO A1). To evaluate the prevalence of autoantibodies against CRP, SAP, MBL, APO A1, and C1q among SLE patients, and their relationship with disease activity, a total of 150 SLE patients were screened for the presence of elevated antibody titers against C1q, CRP, SAP, MBL, and APO A1, utilizing the enzyme-linked immunosorbent assay (ELISA) method. Disease activity was assessed using the ECLAM or SLEDAI scores. The study population comprised two groups of patients: 100 patients with quiescent disease (median ECLAM score 2) comprised the first group, and 50 patients with active disease (median SLEDAI score 16) comprised group 2. Elevated titers of anti-CRP antibodies were significantly elevated only in group 1 (10% versus 4% of controls). Antibodies against SAP were evaluated only among patients in group 1, and were found at a significant high prevalence (20%). Elevated titers of anti-MBL antibodies were significantly elevated only in group 1 (15% versus 3.6%); and antibodies directed against APO A1 were significantly elevated in 21% of group 1, and 50% of group 2 patients. Elevated titers of anti-C1q were evaluated only in group 2, and were found at a significant prevalence of 66%. Significant correlation with disease activity was found only for anti-APO A1 antibodies, and only in group 1. Several patients harbored more than one of the autoantibodies tested. In patients with SLE, autoantibodies directed against protective molecules, that is, acute-phase proteins involved in the disposal of cellular and nuclear debris, can be detected. These autoantibodies may play a pathogenic role in the development or perpetuation of autoimmunity in SLE.
authors: Center for Autoimmune Diseases and Department of Medicine B, Chaim Sheba Medical Center, Tel-Hashomer, Israel. shoenfel@post.tau.ac.il
authors: Yehuda
authors: Y
authors: Shoenfeld
authors: Martine
authors: M
authors: Szyper-Kravitz
authors: Torsten
authors: T
authors: Witte
authors: Andrea
authors: A
authors: Doria
authors: Akito
authors: A
authors: Tsutsumi
authors: Abe
authors: A
authors: Tatsuya
authors: Jean-Michel
authors: JM
authors: Dayer
authors: Pascale
authors: P
authors: Roux-Lombard
authors: Lionel
authors: L
authors: Fontao
authors: Cees G M
authors: CG
authors: Kallenberg
authors: Marc
authors: M
authors: Bijl
authors: Torsten
authors: T
authors: Matthias
authors: Abigail
authors: A
authors: Fraser
authors: Gisele
authors: G
authors: Zandman-Goddard
authors: Miri
authors: M
authors: Blank
authors: Boris
authors: B
authors: Gilburd
authors: Pier Luigi
authors: PL
authors: Meroni
mesh_terms: D016632:Apolipoprotein A-I / Q000276:immunology; D017209:Apoptosis / Q000276:immunology; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D001324:Autoantigens / Q000276:immunology*; D002097:C-Reactive Protein / Q000276:immunology; D015922:Complement C1q / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000276:immunology* / Q000503:physiopathology; D037241:Mannose-Binding Lectins / Q000276:immunology; D000683:Serum Amyloid P-Component / Q000276:immunology
chemical_list: D016632:Apolipoprotein A-I; D001323:Autoantibodies; D001324:Autoantigens; D037241:Mannose-Binding Lectins; D000683:Serum Amyloid P-Component; D015922:Complement C1q; D002097:C-Reactive Protein