Woda B A, Handler E S, Greiner D L, Reynolds C, Mordes J P, Rossini A A
Department of Pathology, University of Massachusetts Medical Center, Worcester 01655.
Diabetes. 1991 Apr;40(4):423-8. doi: 10.2337/diab.40.4.423.
Diabetes-prone (DP) BB rats develop spontaneous autoimmune insulin-dependent diabetes mellitus (IDDM). The cell populations involved in the expression of diabetes are not precisely known but probably include natural killer (NK) cells, macrophages, and T lymphocytes. Because the DP rat has few lymphocytes of the CD5+/CD+ phenotype, cytotoxic T lymphocytes (Tc) are not believed to be important in the process. Diabetes-resistant (DR) BB rats that are depleted of RT6+ T lymphocytes also become diabetic and provide an additional model of IDDM. We report that diabetes in DR rats depleted of RT6+ T lymphocytes is prevented by the concomitant depletion of either the CD5+ or the CD8+ population. In contrast, coadministration of anti-asialogangliosideM1 (alpha-ASGM1), an antiserum that principally recognizes NK cells, failed to prevent hyperglycemia in RT6-depleted rats. We propose that the initiation of diabetes in both DP and RT6-depleted DR rats is T-lymphocyte dependent. However, the final common pathway leading to autoimmune beta-cell destruction in IDDM may be different in these models. The RT6-depleted DR rat requires a cell that is sensitive to anti-CD8 (possibly a Tc), whereas the DP rat requires an anti-ASGM1-sensitive cell.
易患糖尿病（DP）的BB大鼠会自发发展为自身免疫性胰岛素依赖型糖尿病（IDDM）。参与糖尿病表达的细胞群体尚不完全清楚，但可能包括自然杀伤（NK）细胞、巨噬细胞和T淋巴细胞。由于DP大鼠中具有CD5+/CD+表型的淋巴细胞很少，因此细胞毒性T淋巴细胞（Tc）在这一过程中被认为并不重要。去除RT6+ T淋巴细胞的抗糖尿病（DR）BB大鼠也会患糖尿病，这提供了另一种IDDM模型。我们报告，去除RT6+ T淋巴细胞的DR大鼠中的糖尿病可通过同时去除CD5+或CD8+群体来预防。相比之下，共同给予抗唾液酸神经节苷脂M1（α-ASGM1）（一种主要识别NK细胞的抗血清）未能预防去除RT6的大鼠出现高血糖。我们提出，DP大鼠和去除RT6的DR大鼠中糖尿病的起始均依赖于T淋巴细胞。然而，在这些模型中，导致IDDM中自身免疫性β细胞破坏的最终共同途径可能有所不同。去除RT6的DR大鼠需要一种对抗CD8敏感的细胞（可能是Tc），而DP大鼠需要一种对抗ASGM1敏感的细胞。
