Boitard C, Larger E, Timsit J, Sempe P, Bach J F
INSERM U25, Hôpital Necker, Paris, France.
Diabetologia. 1994 Sep;37 Suppl 2:S90-8. doi: 10.1007/BF00400831.
Insulin-dependent diabetes develops as a consequence of the selective destruction of insulin-producing cells by an autoimmune reaction. However, the precise series of events which trigger anti-islet autoreactive T cells is still being investigated. Major issues will need to be raised before a comprehensive view of the anti-islet autoimmune reaction can be delineated. These include defining the primary site of activation of autoreactive lymphocytes and exploring hypotheses to explain the chronicity of the diabetes process. These issues all relate with the more general dilemma of the actual role of the islets of Langerhans in breaking self tolerance to beta-cell antigens. By studying non-obese diabetic mice deprived of beta cells following a single injection of a high dose of alloxan at 3 weeks of age, we recently obtained evidence that the activation of autoreactive T cells requires the presence of target islet cells in order to develop.
胰岛素依赖型糖尿病是由自身免疫反应选择性破坏胰岛素产生细胞所致。然而，触发抗胰岛自身反应性T细胞的确切事件序列仍在研究中。在能够勾勒出抗胰岛自身免疫反应的全面图景之前，需要提出一些主要问题。这些问题包括确定自身反应性淋巴细胞的主要激活部位，并探索各种假说来解释糖尿病进程的慢性特征。这些问题都与胰岛在打破对β细胞抗原的自身耐受性方面的实际作用这一更为普遍的困境相关。通过研究在3周龄时单次注射高剂量四氧嘧啶后β细胞被剥夺的非肥胖糖尿病小鼠，我们最近获得了证据，表明自身反应性T细胞的激活需要靶胰岛细胞的存在才能发生。
