Jørgensen A, Wiencke A K, la Cour M, Kaestel C G, Madsen H O, Hamann S, Lui G M, Scherfig E, Prause J U, Svejgaard A, Odum N, Nissen M H, Röpke C
Institute of Medical Anatomy Section A, University of Copenhagen, Denmark.
Invest Ophthalmol Vis Sci. 1998 Aug;39(9):1590-9.
The immune privilege of the eye has been thought to be dependent on physical barriers and absence of lymphatic vessels. However, the immune privilege may also involve active immunologic processes, as recent studies have indicated. The purpose of the present study was to investigate whether human retinal pigment epithelial (RPE) cells can induce apoptosis in activated T cells.
Fas ligand (FasL) expression was detected by flow cytometry and immunohistochemistry. Cultured RPE cells were cocultured with T-cell lines and peripheral blood lymphocytes for 6 hours to 2 days. Induction of apoptosis was detected by 7-amino-actinomycin D and annexin V staining.
Retinal pigment epithelial cells expressed FasL and induced apoptosis in activated Fas+ T cells. Blocking of Fas-FasL interaction with antibody strongly inhibited RPE-mediated T-cell apoptosis. Retinal pigment epithelial cells induced apoptosis in several activated T-cell populations and T-cell lines, including T-cell antigen receptor (TCR)-CD3-negative T-cell lines. In contrast, RPE cells induced little or no apoptosis in resting peripheral T cells. Major histocompatibility complex (MHC) class II monoclonal antibodies, which block alloactivation, had no inhibitory effect on RPE-mediated T-cell apoptotic responses in MHC class II-specific CD4+ T-cell lines.
Retinal pigment epithelial cells express FasL and induce TCR-independent apoptosis in activated human T cells through Fas-FasL interaction. Retinal pigment epithelial cells may constitute an immunologic functional barrier against potentially harmful T cells.
眼睛的免疫赦免一直被认为依赖于物理屏障和淋巴管的缺失。然而，正如最近的研究所表明的，免疫赦免也可能涉及主动免疫过程。本研究的目的是调查人类视网膜色素上皮（RPE）细胞是否能诱导活化的T细胞凋亡。
通过流式细胞术和免疫组织化学检测Fas配体（FasL）的表达。将培养的RPE细胞与T细胞系和外周血淋巴细胞共培养6小时至2天。通过7-氨基放线菌素D和膜联蛋白V染色检测凋亡的诱导情况。
视网膜色素上皮细胞表达FasL并诱导活化的Fas+ T细胞凋亡。用抗体阻断Fas-FasL相互作用可强烈抑制RPE介导的T细胞凋亡。视网膜色素上皮细胞在几个活化的T细胞群体和T细胞系中诱导凋亡，包括T细胞抗原受体（TCR）-CD3阴性T细胞系。相比之下，RPE细胞在静止的外周T细胞中几乎不诱导或不诱导凋亡。阻断同种异体活化的主要组织相容性复合体（MHC）II类单克隆抗体对MHC II类特异性CD4+ T细胞系中RPE介导的T细胞凋亡反应没有抑制作用。
视网膜色素上皮细胞表达FasL，并通过Fas-FasL相互作用在活化的人类T细胞中诱导不依赖TCR的凋亡。视网膜色素上皮细胞可能构成针对潜在有害T细胞的免疫功能屏障。
