Neither B Lymphocytes Nor Antibodies Directed Against Self Antigens of the Islets of Langerhans Are Required for Development of Virus-Induced Autoimmune Diabetes

摘要: We evaluated the role of humoral arm immune response in causing or contributing to virus-induced diabetes. Transgenic mice expressing nucleoprotein (NP) glycoprotein (GP) lymphocytic choriomeningitis virus (LCMV) under control rat insulin promoter (RIP) pancreatic β cells (RIP-LCMV) and RIP-LCMV with genetic dysfunction B (RIP-LCMV × μ MT/μ MT ) were compared for development diabetes after challenge LCMV. After inoculation LCMV, T lymphocytes macrophages infiltrated into islets mice, over 50% these generated Abs against host glutamate decarboxylase. However, neither nor autoantibodies played a direct initiation, kinetics, severity as judged by comparing disease littermates whose functional genetically eliminated. Furthermore, quality quantity lymphocyte macrophage infiltration was similar cell-deficient non-B mice. Although islet Ags had no influence on pathogenesis insulin-dependent (type 1) mellitus, it served prediabetes marker, such often elevated before onset disease. Hence, model is not only useful understanding pathogenetic mechanisms how are destroyed spared but also evaluating therapeutic strategies clinical