Transforming growth factor-β and interleukin-10 subvert alloreactive delayed type hypersensitivity in cardiac allograft acceptor mice
Transforming growth factor-β and interleukin-10 subvert alloreactive delayed type hypersensitivity in cardiac allograft acceptor mice
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DOI：
10.1097/00007890-200004150-00055
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发表时间：
2000-04-15
期刊：
影响因子：
6.2
通讯作者：
Orosz, CG
中科院分区：
文献类型：
--
作者：
Bickerstaff, AA;VanBuskirk, AM;Orosz, CG
我们以前曾报道过，用硝酸镓（GN）临时治疗心脏同种异体移植物受者会导致移植物存活不确定，并且不能产生供者反应性迟发型超敏反应（DTH）。我们报告，无论是转化生长因子β（TGF β）或白细胞介素-10（IL-10）的抗体可以揭示DTH反应供体同种异体抗原在心脏移植受体小鼠。未被TGF β反应性抗体覆盖的DTH应答可被外源性IL 10阻断，未被IL 10反应性抗体覆盖的DTH应答可被外源性TGF β阻断。这些数据表明，同种异体移植受体小鼠是完全致敏的，并准备使供体反应性细胞介导的免疫应答。然而，这种反应被供体同种异体抗原依赖性机制所破坏，该机制涉及TGF β和IL 10，这反过来又干扰局部细胞介导的免疫反应。
We have previously reported that temporary treat ment of cardiac allograft recipients with gallium nitrate (GN) results in indefinite graft survival, and the inability to mount donor-reactive delayed type hypersensitivity (DTH) responses. We report that antibodies to either transforming growth factor-beta (TGF beta) or interleukin-10 (IL10) can uncover DTH responses to donor alloantigens in cardiac allograft acceptor mice. The DTH responses uncovered with TGF beta-reactive antibodies can be blocked by exogenous IL10, and those uncovered with IL10-reactive antibodies can be blocked by exogenous TGF beta. These data demonstrate that allograft acceptor mice are fully allosensitized, and poised to make donor-reactive cell-mediated immune responses. However, such responses are subverted by a donor alloantigen-dependent mechanism that involves TGF beta and IL10, which in turn interfere with local cell-mediated immune responses.