Sarkar P, Crisá L, McKeever U, Bortell R, Handler E, Mordes J P, Waite D, Schoenbaum A, Haag F, Koch-Nolte F
Diabetes Division, University of Massachusetts Medical Center, Worcester.
Autoimmunity. 1994;18(1):15-22. doi: 10.3109/08916939409014675.
T cells expressing the RT6 surface alloantigen perform important immunoregulatory functions in the rat. Diabetes prone (DP) BB rats are deficient in circulating RT6+ T cells and develop spontaneous autoimmune diabetes mellitus. Transfusions leading to engraftment of RT6+ T cells prevent the disease. Coisogenic diabetes resistant (DR) BB rats do circulate RT6+ T cells and are free of disease. We investigated the basis for the deficiency of RT6+ T cells in the DP-BB rat and made the following observations. 1. Thymectomy causes the rapid loss of most peripheral T cells in the DP-BB rat. 2. Concomitant with the loss of T cells is the total loss of mRNA encoding RT6. 3. In contrast to the effects observed in peripheral lymphoid tissues, thymectomy does not lead to a detectable loss in RT6+ protein found in the small intestine. We conclude that the deficiency of RT6+ peripheral T cells in the DP-BB rat is due either to their short life span or to their reduced proliferative capacity following release from the thymus.
表达RT6表面同种异体抗原的T细胞在大鼠中发挥重要的免疫调节功能。糖尿病易感（DP）BB大鼠循环中的RT6 + T细胞缺乏，并会发展为自发性自身免疫性糖尿病。输注导致RT6 + T细胞植入可预防该病。同基因糖尿病抗性（DR）BB大鼠确实循环有RT6 + T细胞且无疾病。我们研究了DP - BB大鼠中RT6 + T细胞缺乏的原因，并得出以下观察结果。1. 胸腺切除导致DP - BB大鼠中大多数外周T细胞迅速丢失。2. 与T细胞丢失同时发生的是编码RT6的mRNA完全丢失。3. 与在外周淋巴组织中观察到的效应相反，胸腺切除不会导致小肠中发现的RT6 + 蛋白有可检测到的丢失。我们得出结论，DP - BB大鼠中RT6 + 外周T细胞的缺乏要么是由于它们的寿命短，要么是由于它们从胸腺释放后增殖能力降低。
