作者: Andrew L. Rankin , Amy J. Reed , Soyoung Oh , Cristina Cozzo Picca , Heath M. Guay
DOI: 10.4049/JIMMUNOL.180.2.833
关键词:
摘要: We have examined processes leading to the spontaneous development of autoimmune inflammatory arthritis in transgenic mice containing CD4+ T cells targeted a nominal Ag (hemagglutinin (HA)) and coexpressing HA driven by MHC class II promoter. Despite being subjected multiple tolerance mechanisms, autoreactive accumulate periphery these promote systemic proinflammatory cytokine production. The majority spontaneously develop arthritis, which is accompanied an enhanced regional immune response lymph nodes draining major joints. Arthritis B cell activation; however, neither nor Ab required for development, since disease develops cell-deficient background. Moreover, also recombinase activating gene-deficient background, indicating that process recognizing neo-self Ag. These findings show single self-Ag, expressed systemically distributed APCs, can induce via mechanism independent their ability provide help autoantibody