Mowat A M, Borland A, Parrott D M
Transplantation. 1986 Feb;41(2):192-8.
This study has examined the nature of the T lymphocytes and the alloantigens that induce the intestinal phase of graft-versus-host reaction in unirradiated F1 mice. Parental spleen cells were depleted of T cells subsets by treatment with anti-Lyt monoclonal antibodies and complement, and we show that Lyt 2- cells alone induce the increased lymphocytic infiltration of the epithelium that characterizes the intestinal graft-versus-host reaction. Lyt 2- cells are also required to induce some of the associated crypt hyperplasia, but the full crypt changes require both Lyt 2- and Lyt 2+ T cells. In intra-H-2 recombinant congenic F1 mice with graft-versus-host reaction, a disparity at the I-A locus was alone sufficient and necessary for crypt hyperplasia and increased intraepithelial lymphocyte counts, while an I-J incompatibility led to suppression of both these indices. The results support the hypothesis that the intestinal pathology of acute GVHD is induced by class II MHC-restricted delayed-type hypersensitivity effector T cells.
本研究检测了未受照射的F1小鼠中引发移植物抗宿主反应肠道期的T淋巴细胞的性质以及同种异体抗原。通过用抗Lyt单克隆抗体和补体处理,去除亲代脾细胞中的T细胞亚群,我们发现单独的Lyt 2-细胞可诱导上皮淋巴细胞浸润增加,这是肠道移植物抗宿主反应的特征。诱导一些相关的隐窝增生也需要Lyt 2-细胞,但完整的隐窝变化需要Lyt 2-和Lyt 2+ T细胞。在发生移植物抗宿主反应的H-2重组近交F1小鼠中,I-A位点的差异单独对于隐窝增生和上皮内淋巴细胞计数增加是充分且必要的,而I-J不相容性导致这两个指标均受到抑制。这些结果支持以下假说:急性移植物抗宿主病的肠道病理是由II类主要组织相容性复合体限制的迟发型超敏反应效应T细胞诱导的。