Cole B C
Department of Internal Medicine, University of Utah College of Medicine, Salt Lake City 84132.
Isr J Med Sci. 1987 May;23(5):496-502.
At least three genes are now known to influence T-lymphocyte activation induced by the soluble mitogen derived from Mycoplasma arthritidis (MAM). The I-E region of the murine major histocompatibility complex (MHC) codes for the synthesis of the E alpha chain of the I-E molecule, which acts as a receptor for MAM. Mouse, rat and human E alpha molecules have a similar structure, and lymphocytes from all of these species can be activated by MAM. However, lymphocytes from the BN rat, which also express this molecule, fail or respond only weakly to MAM and lectin mitogens due to the influence of a non-MHC gene(s). The RIIIS mouse strain also expresses the E alpha receptor site for MAM, but possesses a recessive non-MHC gene(s) that is associated with an inability of lymphocytes to respond to MAM without influencing their responses to lectin mitogens. There is evidence that in the BN rat and the RIIIS mouse there is a defect in T cell interactions with the mitogen/accessory cells complex. Evidence is also presented that T-lymphocyte activation in vivo may predispose mice to the toxic and necrotizing properties of viable M. arthritidis.
目前已知至少有三个基因会影响由关节炎支原体（MAM）衍生的可溶性促细胞分裂剂诱导的T淋巴细胞活化。小鼠主要组织相容性复合体（MHC）的I-E区域编码I-E分子的Eα链的合成，该分子作为MAM的受体。小鼠、大鼠和人类的Eα分子结构相似，来自所有这些物种的淋巴细胞都可以被MAM激活。然而，同样表达这种分子的BN大鼠的淋巴细胞由于非MHC基因的影响，对MAM和凝集素促细胞分裂剂反应失败或反应微弱。RIIIS小鼠品系也表达MAM的Eα受体位点，但拥有一个隐性非MHC基因，该基因与淋巴细胞无法对MAM作出反应有关，而不影响它们对凝集素促细胞分裂剂的反应。有证据表明，在BN大鼠和RIIIS小鼠中，T细胞与促细胞分裂剂/辅助细胞复合体的相互作用存在缺陷。还有证据表明，体内T淋巴细胞活化可能使小鼠易受活的关节炎支原体的毒性和坏死特性影响。
