作者: Terry B. Strom , Vicki E. Kelley
DOI: 10.1038/KI.1989.86
关键词: Immunology 、 Antigen 、 Immune system 、 Insulitis 、 Monoclonal antibody 、 Biology 、 CD8 、 Antibody 、 T cell 、 NOD mice
摘要: Although vigorous immune responses are required to preserve a healthy state, plethora of undesired reactions can also occur, such as systemic autoimmunity, allograft rejection and nephritogenic processes. T cells the dominant cell type present in many these unwanted responsible for tissue damage. For example, insulin dependent diabetes mellitus (IDDM) both CD4+ CD8+ lymphocytes infiltrate islets trigger immunologically-mediated beta destruction [1–7]. Studies animal models human disease indicate that insulitis requires intact function. Splenic obtained from diabetic NOD mice transfer younger non-diabetic [8]. Both state hosts young syngeneic animals [9, 10]. Treatment experimental with anti-T antibodies [11, 12], anti-CD4 monoclonal [7], anti-IL-2 receptor [13], neonatal thymectomy [14], total lymphoid irradiation [15] or cyclosporine [16, 17] all prevent progressive loss. Many undesirable characteristic IDDM be identified tissues inflammatory sites other autoimmune diseases during states. Thus, it is not surprising therapeutic strategies directed toward eliminating blocking functions abort variety