Babu P G, Saraswathi N K, John T J
Department of Virology & Immunology, Christian Medical College Hospital, Vellore, India.
Indian J Exp Biol. 1992 Sep;30(9):769-74.
Earlier we had described a dual aetiology diabetes mellitus (DADM) in mice injected with a sub-diabetogenic dose of streptozotocin (SD-SZN) and afterwards infected with coxsackie B3 virus (CBV). Further experiments were conducted to understand the mechanism of diabetogenesis. In in vitro stimulation and proliferation tests, the splenic lymphocytes (SLC) of mice given either SD-SZN or CBV infection showed lower responses to two T cell mitogens than those of control mice, indicating an immunosuppressive effect. Unexpectedly, SLC of mice given both SD-SZN and CBV showed enhanced response, indicating immunoactivation; they were not stimulated to proliferation in response to CBV antigen, indicating that the immunoactivation was not directed against CBV, but against streptozotocin or cellular elements. When mice were depleted of T cells by injecting with anti-thymocyte serum, the diabetogenic effect of SD-SZN and CBV infection was abrogated, without diminishing the replication of virus in the pancreas. Thus beta cell injury in DADM appears to be T cell-mediated.
早些时候，我们描述了在注射亚糖尿病剂量链脲佐菌素（SD - SZN）后感染柯萨奇B3病毒（CBV）的小鼠中的双病因糖尿病（DADM）。为了解糖尿病发生机制，我们进行了进一步实验。在体外刺激和增殖试验中，接受SD - SZN或CBV感染的小鼠的脾淋巴细胞（SLC）对两种T细胞有丝分裂原的反应低于对照小鼠，表明存在免疫抑制作用。出乎意料的是，同时接受SD - SZN和CBV的小鼠的SLC显示出增强的反应，表明免疫激活；它们并未因CBV抗原刺激而增殖，表明这种免疫激活并非针对CBV，而是针对链脲佐菌素或细胞成分。当通过注射抗胸腺细胞血清使小鼠T细胞耗竭时，SD - SZN和CBV感染的致糖尿病作用被消除，而胰腺中病毒的复制并未减少。因此，DADM中的β细胞损伤似乎是由T细胞介导的。
