Doherty P C, Dunlop M B, Parish C R, Zinkernagel R M
J Immunol. 1976 Jul;117(1):187-90.
Capacity to transfer adoptively fatal lymphocytic choriomeningitis (LCM) to immunosuppressed, virus-infected recipients is a property of H-2 compatible, non-Ig-bearing virus-immune lymphocytes. Severe meningitis is recognized when donor and recipient share at least one allele at either H-2K or H-2D. Presence of unshared H-2 genes is not obviously inhibitory, and identity at the immune response (Ir) region of the H-2 gene complex is neither sufficient nor necessary. The same constraint applies to cytotoxic T cell activity in vitro; lymphocytes and virus-infected targets must be compatible for a minimum of one allele mapping at H-2K or H-2D. The present findings thus support the concept that populations of T cells, which are cytotoxic in vitro, also mediate inflammatory process in vivo and are a major, if not the only, effector population in murine LCM.
将致死性淋巴细胞性脉络丛脑膜炎（LCM）过继转移至免疫抑制的病毒感染受体的能力是H-2相容、不携带免疫球蛋白的病毒免疫淋巴细胞的一种特性。当供体和受体在H-2K或H-2D位点至少共享一个等位基因时，会发生严重的脑膜炎。未共享的H-2基因的存在并无明显抑制作用，并且H-2基因复合体免疫反应（Ir）区域的一致性既非充分条件也非必要条件。同样的限制也适用于体外细胞毒性T细胞活性；淋巴细胞和病毒感染的靶细胞必须至少在H-2K或H-2D位点的一个等位基因上相容。因此，目前的研究结果支持了这样一种概念，即在体外具有细胞毒性的T细胞群体在体内也介导炎症过程，并且是小鼠LCM中主要的效应细胞群体，即便不是唯一的效应细胞群体。
