Yang Y, Charlton B, Shimada A, Dal Canto R, Fathman C G
Stanford University School of Medicine, Division of Immunology and Rheumatology, California 94305-5111, USA.
Immunity. 1996 Feb;4(2):189-94. doi: 10.1016/s1074-7613(00)80683-4.
To examine the hypothesis that a single initiating antigen was recognized by a monoclonal T cell population leading to subsequent inflammatory insulitis in non-obese (NOD) mouse islets, we examined the T cell receptor TCR V beta repertoire of islet-infiltrating T cells in very young (2-week-old) NOD mice. In independent experiments, we repeatedly identified one monoclonal TCR V-beta 8.2 gene product expressed by T lymphocytes infiltrating the islets of NOD mice at 2 weeks of age. The resultant inflammatory response quickly obscures the monoclonal nature of the initiating event. These data suggest that autoimmune diabetes in NOD mice may be initiated by recognition of a single autoantigen.
为了检验单一起始抗原被单克隆T细胞群体识别从而导致非肥胖(NOD)小鼠胰岛随后发生炎症性胰岛炎这一假说,我们检测了非常年幼(2周龄)NOD小鼠胰岛浸润性T细胞的T细胞受体(TCR)Vβ谱型。在独立实验中,我们反复鉴定出一种由2周龄NOD小鼠胰岛浸润性T淋巴细胞表达的单克隆TCR V-β8.2基因产物。由此产生的炎症反应很快掩盖了起始事件的单克隆性质。这些数据表明,NOD小鼠的自身免疫性糖尿病可能由单一自身抗原的识别引发。