Role of lymphokine in islet allograft rejection.
Role of lymphokine in islet allograft rejection.
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淋巴因子在胰岛同种异体移植排斥中的作用。
DOI：
10.1097/00007890-199003000-00025
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发表时间：
1990
期刊：
影响因子：
6.2
通讯作者：
Lafferty,KJ
中科院分区：
文献类型：
--
作者：
Hao,LM;Wang,Y;Gill,RG;LaRosa,FG;Talmage,DW;Lafferty,KJ
启动的CD8 T细胞将同种异体移植物免疫转移到已建立的同种异体胰岛移植物。然而，这一过程被环孢素抑制，表明胰岛移植排斥反应需要淋巴因子的产生。同种异体反应性T细胞克隆L3会传递同种异体移植物免疫，这一过程对CsA也很敏感。L3克隆产生γ -干扰素和肿瘤坏死因子，但不产生IL-2和IL-3。因此，后一种淋巴因子在排斥过程中是不需要的。移植前用[γ]-IFN对胰岛组织进行预处理，增加了胰岛组织上I类主要组织相容性复合体抗原的密度，CsA不再能够阻断mhc诱导的同种异体反应性T细胞对该组织的破坏。我们得出结论，[γ]-IFN，可能还有TNF，在胰岛移植排斥过程中协同细胞毒功能。
Primed CD8 T cells transfer allograft immunity to an established islet allograft. However, the process is inhibited by cyclosporine, suggesting that lymphokine production is required for islet graft rejection. The alloreactive T cell clone L3 will transfer allograft immunity, and this process is also sensitive to CsA. The L3 clone produces gamma-interferon and tumor necrosis factor but not IL-2 and IL-3. It follows therefore that the latter lymphokines are not required for the rejection process. Pretreatment of islet tissue with [gamma]-IFN prior to grafting increases the density of the class I major histocompatibility complex antigen on the islet tissue, and CsA can no longer block the destruction of this MHC-induced tissue by primed alloreactive T cells. We conclude that [gamma]-IFN, and possibly TNF, act cooperatively with cytotoxic function in the process of islet allograft rejection.