作者: Micah T. McClain , Brian D. Poole , Benjamin F. Bruner , Kenneth M. Kaufman , John B. Harley
DOI: 10.1002/ART.21682
关键词: Autoantibody 、 Immune system 、 Antigen 、 Medicine 、 Antibody 、 Virology 、 Autoimmunity 、 Autoimmune disease 、 Epitope 、 Immunology 、 Systemic lupus erythematosus
摘要: Objective New examples support the concept that host immune responses to pathogenic organisms can act as nidus for autoimmunity. Two such implicate Epstein-Barr virus (EBV) in systemic lupus erythematosus (SLE), i.e., data consistent with SLE anti-Sm and anti–60-kd Ro autoantibodies emerging from distinct humoral nuclear antigen 1 (EBNA-1). We undertook this study further test whether response EBNA-1 is a risk factor pediatric SLE. Methods Sera patients healthy matched controls were tested anti–EBNA-1 by Western blotting enzyme-linked immunosorbent assay (ELISA). To define fine specificity of their response, fragments maximally overlapping unique octapeptides modified ELISAs. Results All 36 patient sera recognized EBNA-1, while only 25 EBV-positive targeted (P < 0.005). Epitope mapping revealed was less restricted than normal individuals. Meanwhile, no significant differences between control observed other herpesviruses or binding sequential epitopes cytomegalovirus immediate-early EBNA-2. Conclusion Anti–EBNA-1 antibodies are associated pediatric-onset SLE. Furthermore, an altered characteristic SLE, has been found may be important susceptibility factor.