EFFECTS OF GRAFT VS HOST REACTIONS ON CELL-MEDIATED IMMUNITY

亲本转F1代移植物抗宿主反应（GVHR）的长期效应 通过以下脾T细胞标志物和功能进行了研究， GVHR诱导后18个月。尽管有足够的数量 表达正常补体T淋巴细胞标记的T细胞， 这些细胞仍然不能产生MHC自身限制的、CD 4介导的T细胞， 助手的回答这种缺陷不是由于抑制或缺陷， 抗原呈递细胞功能。供体嵌合体分析 亲本到F1代GVHR表明了三个阶段的再增殖：扩增 供体T细胞的阶段;宿主细胞破坏的阶段;和供体T细胞的阶段。 再增殖期，其中观察到广泛的供体细胞再增殖。 研究了诱导GVHR的供体T细胞的T细胞受体库 通过Vbeta分析。观察到表达Vbeta的供体T细胞 抗宿主反应性的标记物在GVHR期间被选择性扩增。Vbeta 分析也被用来调查可能的协同作用之间的I类 GVHR和供体-抗宿主m1识别。发现供体-抗宿主 I类H-2和m1 s（a）的识别导致急性GVHR， 与m1 s反应的V β T细胞受体的优先扩增（a）。 这些V β T细胞的消耗导致供体嵌合体减少，但 而不是消除GVH诱导的免疫缺陷。

The long-term effects of parent-into-F1 graft-versus-host reaction (GVHR) was investigated by following splenic T cell markers and function for up to 18 months after GVHR induction. Despite the appearance of adequate numbers of T cells which expressed the normal compliment of T lymphocyte markers, these cells still failed to generate MHC self-restricted, CD4-mediated T helper responses. This defect was not due to suppression or a defect in antigen-presenting cell function. Analysis of donor chimerism in parent-into-F1 GVHR indicated three phases of repopulation: an expansion phase of donor T cells; a phase of host cell destruction; and a donor repopulation phase in which extensive donor cell repopulation is observed. Donor T cells that induce GVHR were studied for T cell receptor repertoire by Vbeta analyses. It was observed that donor T cell expressing the Vbeta markers of antihost reactivity were selectively expanded during GVHR. Vbeta analysis was also used to investigate the possible synergy between class I GVHR and donor-antihost m1s recognition. It was found that donor-antihost recognition of class I H-2 and m1s(a) resulted in acute GVHR, and preferential expansion of the Vbeta T cell receptor reactive with m1s(a). Depletion of these Vbeta T cells resulted in reduced donor chimerism, but not in abrogation of GVH-induced immune deficiency.