Hunt H D, Lubaroff D M
Department of Microbiology, University of Iowa, Iowa City.
Cell Immunol. 1992 Aug;143(1):194-211. doi: 10.1016/0008-8749(92)90016-i.
The functional and phenotypic heterogeneity of the rat peripheral T lymphocyte antigen RT6 has been examined. The in vivo popliteal graft-vs-host reaction (GvHR), in vitro MLR, and the generation and effector populations of cytotoxic T lymphocyte were used to examine the response of RT6-positive (RT6+) or -negative (RT6-) subsets of CD4 and CD8 T cells to alloantigen. T lymphocytes with the CD4+RT6+ surface phenotype are necessary and sufficient for inducing a strong GvHR. T lymphocytes with the CD4+RT6-, CD8+RT6+, and CD8+RT6- surface phenotypes do not contribute or induce a strong GvHR. Both the CD4+RT6+ and the CD4+RT6- T cells proliferate in the MLR assay. CTL precursors are a mixture of CD8+RT6+ and CD8+RT6- phenotypes, but only cells bearing the RT6- phenotype are potent CTL effector cells. Data presented in this paper also demonstrate that the RT6.1 alloantigen, present on the majority of rat T cells, modulates on cortisone-resistant thymocytes (CRT) and peripheral T cells. Although freshly isolated CRTs do not express the RT6.1 epitope, RT6+ cells develop when CRTs are placed into culture. Peripheral T cells that are RT6- will also become RT6+ in culture. Stimulation of T cell cultures with a mitogen causes the loss of the RT6.1 antigen, as detected by the DS4.23 mAb. The effect is more pronounced in cultures of CRTs than peripheral T cells. Following a return to a nonactivated state, the T cells reexpress RT6. The loss and reexpression of RT6 may be related to activation and/or differentiation of T cells.
已对大鼠外周T淋巴细胞抗原RT6的功能和表型异质性进行了研究。采用体内腘窝移植物抗宿主反应（GvHR）、体外混合淋巴细胞反应（MLR）以及细胞毒性T淋巴细胞的产生和效应群体，来检测CD4和CD8 T细胞的RT6阳性（RT6+）或阴性（RT6-）亚群对同种异体抗原的反应。具有CD4+RT6+表面表型的T淋巴细胞对于诱导强烈的GvHR是必要且充分的。具有CD4+RT6-、CD8+RT6+和CD8+RT6-表面表型的T淋巴细胞对强烈的GvHR无贡献或不能诱导其产生。CD4+RT6+和CD4+RT6- T细胞在MLR试验中均能增殖。细胞毒性T淋巴细胞前体是CD8+RT6+和CD8+RT6-表型的混合物，但只有具有RT6-表型的细胞才是有效的细胞毒性T淋巴细胞效应细胞。本文提供的数据还表明，大多数大鼠T细胞上存在的RT6.1同种异体抗原可调节耐可的松胸腺细胞（CRT）和外周T细胞。尽管新鲜分离的CRT不表达RT6.1表位，但将CRT置于培养中时会形成RT6+细胞。培养中的RT6-外周T细胞也会变成RT6+。用丝裂原刺激T细胞培养物会导致RT6.1抗原丢失，这可通过DS4.23单克隆抗体检测到。这种效应在CRT培养物中比在外周T细胞中更明显。恢复到未激活状态后，T细胞会重新表达RT6。RT6的丢失和重新表达可能与T细胞的激活和/或分化有关。
