Pelletier L, Rossert J, Pasquier R, Villarroya H, Belair M F, Vial M C, Oriol R, Druet P
INSERM U 28, Hôpital Broussais, Paris, France.
Eur J Immunol. 1988 Feb;18(2):243-7. doi: 10.1002/eji.1830180210.
HgCl2 induces autoimmunity in Brown-Norway rats and immunosuppression in Lewis rats. In the latter rats, HgCl2 triggers the proliferation of T suppressor/cytotoxic (OX8+) cells which actively suppress T cell functions. This led us to study the effect of HgCl2 on experimental allergic encephalomyelitis (EAE), a T cell-mediated autoimmune disease obtained following immunization with basic protein (BP). It will be shown that HgCl2 attenuates or even prevents clinical manifestations of EAE and inhibits both the proliferative response of T cells to BP and the anti-BP antibody response. This immunosuppression was not due to a defect at the T helper cell or antigen-processing cell level but to the emergence of T suppressor cells.
氯化汞可在布朗 - 挪威大鼠中诱发自身免疫反应，并在刘易斯大鼠中引起免疫抑制。在后者中，氯化汞触发抑制性/细胞毒性T细胞（OX8 +）的增殖，这些细胞会积极抑制T细胞功能。这促使我们研究氯化汞对实验性自身免疫性脑脊髓炎（EAE）的影响，EAE是一种在用碱性蛋白（BP）免疫后获得的T细胞介导的自身免疫性疾病。结果将表明，氯化汞可减轻甚至预防EAE的临床表现，并抑制T细胞对BP的增殖反应以及抗BP抗体反应。这种免疫抑制并非由于辅助性T细胞或抗原处理细胞水平的缺陷，而是由于抑制性T细胞的出现。
