Specific unresponsiveness in rats with prolonged cardiac allograft survival after treatment with cyclosporine. Mediation of specific suppression by T helper/inducer cells.
Specific unresponsiveness in rats with prolonged cardiac allograft survival after treatment with cyclosporine. Mediation of specific suppression by T helper/inducer cells.
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用环孢菌素治疗后，患有长时间同种异体移植生存的大鼠的特异性无反应性。 T辅助/诱导剂细胞对特定抑制的介导。
DOI：
10.1084/jem.162.5.1683
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发表时间：
1985-11-01
期刊：
影响因子：
--
通讯作者：
Dorsch SE
中科院分区：
文献类型：
--
作者：
Hall BM;Jelbart ME;Gurley KE;Dorsch SE
DA大鼠移植与主要组织相容性复合物不相容的PVG心脏移植物和环孢素（CY）治疗10天不排斥他们的移植物，并制定了一个国家的具体无反应性PVG同种异体移植物。在过继转移测定中测试的来自这些动物的细胞不能恢复PVG移植物排斥，并且能够特异性抑制过继转移的正常淋巴结细胞（LNC）恢复PVG移植物排斥的能力。然而，它们影响了第三方Wistar/Furth（W/F）移植物排斥反应。介导这种效应的淋巴细胞纯化亚群的连续转移试验表明，辅助/诱导亚类的W3/25+ T细胞，当单独注射时，不能恢复排斥反应，并且当与正常LNC或从它们分离的W/25+细胞一起注射时，也能够防止这些细胞产生排斥反应。细胞毒性/抑制子亚类的MRC OX 8 + T细胞、B细胞和来自移植物长期存活的大鼠的血清均不能抑制正常LNC的同种异体移植物反应性，因此未被鉴定为特异性无反应性状态的介质.这些结果表明，特定的无反应性，在大鼠长期存活的移植物，这至少在一定程度上是负责延长移植物存活，是由于在同种异体反应性的辅助/诱导T细胞亚类的改变。这些细胞不仅缺乏启动针对移植物的同种异体抗原的排斥反应的能力，而且具有抑制正常W3/25+细胞这样做的能力。
DA rats grafted with major histocompatibility complex-incompatible PVG heart grafts and treated with cyclosporine (CY) for 10 d do not reject their grafts, and develop a state of specific unresponsiveness toward PVG allografts. Cells from these animals tested in an adoptive transfer assay were incapable of restoring PVG graft rejection, and capable of specifically inhibiting the capacity of adoptively transferred normal lymph node cells (LNC) to do so. They effected third party Wistar/Furth (W/F) graft rejection, however. Adoptive transfer assays with purified subpopulations of the lymphocytes that mediated this effect showed that W3/25+ T cells of the helper/inducer subclass, when injected alone, failed to restore rejection, and were also able, when injected with normal LNC or the W/25+ cells separated from them, to prevent these cells from effecting rejection. MRC OX8+ T cells of the cytotoxic/suppressor subclass, B cells, and serum from rats with long- surviving grafts all failed to inhibit the allograft responsiveness of normal LNC, and thus were not identified as mediators of the state of specific unresponsiveness. These results show that the specific unresponsiveness that develops in rats with long-surviving grafts, and which, in part at least, is responsible for prolonged graft survival, is due to an alteration in the alloreactivity of the helper/inducer subclass of T cells. These cells not only lack the capacity to initiate a rejection response against the alloantigens of the graft, but also have the ability to inhibit the capacity of normal W3/25+ cells to do so.