Human fetal retinal pigment epithelial cells induce apoptosis in allogenic T-cells in a Fas ligand and PGE2 independent pathway.
Human fetal retinal pigment epithelial cells induce apoptosis in allogenic T-cells in a Fas ligand and PGE2 independent pathway.
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人胎儿视网膜色素上皮细胞通过 Fas 配体和 PGE2 独立途径诱导同种异体 T 细胞凋亡。
DOI：
10.1076/ceyr.18.6.430.5269
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发表时间：
1999
影响因子：
2
通讯作者：
vanSeventer,GA
中科院分区：
文献类型：
--
作者：
Rezai,KA;Semnani,RT;Farrokh-Siar,L;Hamann,KJ;Patel,SC;Ernest,JT;vanSeventer,GA
目的探讨人胎视网膜色素上皮细胞（HFRPE）对人T细胞活化的抑制作用。方法将HFRPE细胞与纯化的人T细胞在3种不同的活化试验中孵育：1）同种异体外周血单个核细胞; 2）OKT 3包被的珠粒在辅助细胞存在下; 3）用佛波酯和植物血凝素刺激HFRPE细胞，在所有三种试验中，HFRPE细胞抑制T细胞的活化。HFRPE介导的T细胞抑制机制是细胞凋亡。Fas配体（FasL）/Fas介导的T细胞抑制的作用被排除，因为FasL蛋白或mRNA不能检测到HFRPE细胞与流式细胞术和逆转录聚合酶链反应，分别。此外，HFRPE细胞的抑制作用不能被抗Fas配体或拮抗性抗Fas抗体阻断。此外，HFRPE细胞抑制抗CD 3 mAb介导的从lpr小鼠分离的鼠脾细胞的T细胞增殖。由于吲哚美辛不能恢复T细胞活化，HFRPE细胞的抑制作用不是PGE 2介导的。虽然HFRPE介导的T细胞凋亡是细胞-细胞接触无关的，但它不是由TNF-α、TGF-β或IL-10的分泌诱导的。HFRPE和T-细胞之间的比例有一个主要的影响HFRPE的抑制effect.ConclusionsHFRPE细胞抑制激活的人T-细胞通过诱导T-细胞凋亡的过程中，涉及可溶性因子的分泌。HFRPE介导的T细胞抑制依赖于HFRPE与T细胞之间的比例。这种不确定的T细胞凋亡途径可能在维持视网膜下腔的免疫赦免中发挥作用，并可能降低HFRPE移植后免疫反应的严重程度。
PurposeTo evaluate the inhibitory effect of human fetal retinal pigment epithelium (HFRPE) on the activation of human T-cells.MethodsPure cultures of HFRPE cells were incubated with purified human T-cells in three different activation assays: 1) allogenic peripheral blood mononuclear cells; 2) OKT3 coated beads in the presence of accessory cells; and 3) stimulation with phorbol ester and phytohemagglutinin.ResultsHFRPE cells suppressed the activation of T-cells in all three assays. The mechanism of HFRPE mediated T-cell suppression was apoptosis. The role of Fas ligand(FasL)/Fas-mediated T-cell suppression was excluded, since FasL protein or mRNA could not be detected on HFRPE cells with flow cytometry and by reverse transcriptase polymerase chain reaction, respectively. Additionally, the inhibitory effect of HFRPE cells could not be blocked by anti-Fas ligand or antagonistic anti-Fas antibodies. Moreover, HFRPE cells suppressed the proliferation of anti-CD3 mAb mediated T-cell proliferation of murine splenocytes isolated from lpr mice. The inhibitory effect of HFRPE cells was not PGE 2 mediated, since indomethacin could not restore the T-cell activation. Although the HFRPE mediated T-cell apoptosis was cell-cell contact independent, it was not induced by secretion of TNF-a, TGF-ß, or IL-10. The ratio between HFRPE and T-cells had a major impact on the HFRPE's inhibitory effect.ConclusionsHFRPE cells suppressed the activation of human T-cells by induction of T-cell apoptosis through a process that involves the secretion of soluble factors. The HFRPE mediated T-cell suppression was dependent on the ratio between HFRPE and T-cells. This undefined pathway of T-cell apoptosis may play a role in the maintenance of immune privilege in the subretinal space and may reduce the severity of the immune response after HFRPE transplantation.
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