{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T05:20:45Z","timestamp":1791091245064,"version":"4.1.0"},"reference-count":30,"publisher":"Rockefeller University Press","issue":"1","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2003,7,7]]},"abstract":"<jats:p>A monolayer of pigment epithelium (PE) lines the iris PE (IPE), ciliary body PE, and retina PE of the inner eye, an immune-privileged site. These neural crest-derived epithelial cells participate in ocular immune privilege through poorly defined molecular mechanisms. Murine PE cells cultured from different ocular tissues suppress T cell activation by differing mechanisms. In particular, IPE cells suppress primarily via direct cell to cell contact. By examining surface expression of numerous candidate molecules (tumor necrosis factor receptor [TNFR]1, TNFR2, CD36, CD40, CD47, CD80, CD86, PD-L1, CD95 ligand, and type I interferon receptor), we report that IPE cells uniquely express on their surface the costimulatory molecule CD86. When IPE were blocked with anti-CD86 or were derived from CD80\/CD86 (but not CD80) knockout (KO) mice, the cells displayed reduced capacity to suppress T cell activation. IPE also failed to suppress activation of T cells in the presence of cytotoxic T lymphocyte\u2013associated antigen 4 (CTLA-4) immunoglobulin or if the T cells were obtained from CTLA-4 (but not CD28) KO mice. We conclude that iris pigment epithelial cells constitutively express cell surface CD86, which enables the cells to contact inhibit T cells via direct interaction with CTLA-4. Thus, ocular immune privilege is achieved in part by subversion of molecules that are usually used for conventional immune costimulation.<\/jats:p>","DOI":"10.1084\/jem.20030097","type":"journal-article","created":{"date-parts":[[2003,7,1]],"date-time":"2003-07-01T00:25:43Z","timestamp":1057019143000},"page":"161-171","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":69,"title":["Iris Pigment Epithelium Expressing CD86 (B7-2) Directly Suppresses T Cell Activation In Vitro via Binding to Cytotoxic T Lymphocyte\u2013associated Antigen 4"],"prefix":"10.1084","volume":"198","author":[{"given":"Sunao","family":"Sugita","sequence":"first","affiliation":[{"name":"Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. Wayne","family":"Streilein","sequence":"additional","affiliation":[{"name":"Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2003,6,30]]},"reference":[{"key":"2023072512062604500_BIB1","doi-asserted-by":"crossref","first-page":"428","DOI":"10.1016\/0952-7915(93)90064-Y","volume":"5","year":"1993","journal-title":"Curr. Opin. Immunol."},{"key":"2023072512062604500_BIB2","first-page":"1940","volume":"37","year":"1996","journal-title":"Invest. Ophthalmol. Vis. Sci."},{"key":"2023072512062604500_BIB3","doi-asserted-by":"crossref","first-page":"3557","DOI":"10.4049\/jimmunol.158.8.3557","volume":"158","year":"1997","journal-title":"J. Immunol."},{"key":"2023072512062604500_BIB4","first-page":"72","volume":"73","year":"1999","journal-title":"Chem. 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