Hu H, Möller G, Abedi-Valugerdi M
Department of Immunology, Arrhenius Laboratories for Natural Sciences, Stockholm University, Stockholm, S-10691, Sweden.
J Autoimmun. 1997 Oct;10(5):441-6. doi: 10.1006/jaut.1997.9997.
Autoimmune diseases induced by mercuric chloride are genetically determined, at least one gene being major histocompatibility complex (MHC)-linked. Previously, we showed that in vitro mercury stimulation induced a high proliferative response in lymphocytes from susceptible mice (high-responders) and that the proliferative response could be restored in lymphocytes from low-responders by pretreating the cells with mercury. We also found that the continuous presence of mercury induced IL-2 and IFN-gamma production, while pretreatment with mercury induced IL-4 production. In this study, we showed that anti-MHC class II monoclonal antibodies blocked both the mercury-induced proliferative responses in lymphocytes from high-responders and the restored proliferative responses in low-responders. In addition, anti-MHC class II antibodies also inhibited the mercury-induced IL-2, IFN-gamma and IL-4 cytokine production in vitro. The results demonstrate that MHC class II antigens directly participate in mercury-induced cytokine production and cell activation, and are required at the onset of the initiation.
由氯化汞诱发的自身免疫性疾病是由基因决定的，至少有一个基因与主要组织相容性复合体（MHC）相关。此前，我们发现体外汞刺激可诱导易感小鼠（高反应者）的淋巴细胞产生高增殖反应，并且通过用汞预处理细胞，低反应者淋巴细胞的增殖反应可以恢复。我们还发现汞的持续存在会诱导白细胞介素-2（IL-2）和γ干扰素（IFN-γ）的产生，而汞预处理则会诱导白细胞介素-4（IL-4）的产生。在本研究中，我们发现抗MHC II类单克隆抗体可阻断高反应者淋巴细胞中汞诱导的增殖反应以及低反应者中恢复的增殖反应。此外，抗MHC II类抗体在体外也抑制汞诱导的IL-2、IFN-γ和IL-4细胞因子的产生。结果表明，MHC II类抗原直接参与汞诱导的细胞因子产生和细胞活化，并且在起始阶段就需要它们。
