Pelletier L, Pasquier R, Rossert J, Druet P
Eur J Immunol. 1987 Jan;17(1):49-54. doi: 10.1002/eji.1830170109.
Brown-Norway (BN) rats injected with HgCl2 have been previously shown to develop a variety of autoimmune abnormalities. The susceptibility of BN rats is genetically controlled, and Lewis rats bearing a different RT1 haplotype are resistant. It will be shown in the present study that the number of MRC OX-8+ (suppressor/cytotoxic) cells increases in the spleen and lymph nodes of Lewis rats injected with HgCl2. The responsiveness to T cell mitogens and to alloantigens is concomitantly inhibited. Spleen cells from Lewis rats injected with HgCl2 fail to induce a local graft-vs.-host reaction. Data presented show that MRC OX-8+ cells are involved in the immunosuppression in Lewis rats treated with HgCl2. Furthermore, lymph node cells and MRC OX-8+ cells from these rats are able to inhibit the normal mixed lymphocyte reaction indicating that suppression is active. Thus, HgCl2 is able to trigger immune dysregulation leading either to autoimmunity or to immunosuppression depending upon the genetic background of the rat strain tested.
先前已表明，注射了氯化汞的棕色挪威（BN）大鼠会出现多种自身免疫异常。BN大鼠的易感性受基因控制，而携带不同RT1单倍型的刘易斯大鼠具有抗性。本研究将表明，注射了氯化汞的刘易斯大鼠脾脏和淋巴结中MRC OX - 8 +（抑制/细胞毒性）细胞数量增加。对T细胞有丝分裂原和同种异体抗原的反应性同时受到抑制。注射了氯化汞的刘易斯大鼠的脾细胞不能诱导局部移植物抗宿主反应。所呈现的数据表明，MRC OX - 8 +细胞参与了用氯化汞处理的刘易斯大鼠的免疫抑制。此外，这些大鼠的淋巴结细胞和MRC OX - 8 +细胞能够抑制正常的混合淋巴细胞反应，表明抑制作用是活跃的。因此，根据所测试大鼠品系的遗传背景，氯化汞能够引发免疫失调，导致自身免疫或免疫抑制。
