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Originally published In Press as doi:10.1167/iovs.08-2397 on September 12, 2008
 (Investigative Ophthalmology and Visual Science. 2009;50:273-280.)
© 2009 by The Association for Research in Vision and Ophthalmology, Inc.
doi:10.1167/iovs.08-2397
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PD-L1 Expression on Human Ocular Cells and Its Possible Role in Regulating Immune-Mediated Ocular Inflammation

Wanhua Yang, Haochuan Li, Peter W. Chen, Hassan Alizadeh, Yuguang He, R. Nick Hogan, and Jerry Y. Niederkorn

From the Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, Texas.

PURPOSE. To assess the expression of PD-L1 and PD-L2 on human ocular cells and their potential to regulate ocular inflammation.

METHODS. Five categories of human ocular cells were evaluated for PD-L1 and PD-L2 expression by RT-PCR and flow cytometry. Three normal eyes and an inflamed eye from a patient with sympathetic ophthalmia were examined by immunohistochemistry for in situ PD-L1 expression. The immunomodulatory functions of PD-L1 and PD-L2 were tested by coculturing untreated or IFN-{gamma}–pretreated ocular cells with activated human peripheral blood T cells for 48 hours and assessing T-cell production of IFN-{gamma}, TNF-{alpha}, IL-4, and IL-5 by ELISA and T-cell apoptosis by flow cytometry.

RESULTS. PD-L1 protein was expressed constitutively in 4 of 5 human ocular cell lines, and its expression was significantly upregulated after stimulation by IFN-{gamma}. Moreover, in situ expression of PD-L1 in inflamed ocular tissues was remarkably upregulated compared with normal eyes. Although PD-L2 expression was detectable by flow cytometry on 3 of 5 ocular cell lines, immunohistochemical staining did not show expression of PD-L2 on either normal or inflamed ocular tissues. IFN-{gamma}, TNF-{alpha}, and IL-5 production by activated T cells cocultured with ocular cells was significantly enhanced in the presence of anti–PD-L1 blocking antibody. However, ocular cell–expressed PD-L1 and PD-L2 did not induce T-cell apoptosis.

CONCLUSIONS. PD-L1 expressed on human ocular cells has a presumptive role in controlling ocular inflammation by inhibiting the production of proinflammatory cytokines and a Th2 cytokine by activated T cells. This may represent an important mechanism for maintaining immune privilege in the eye.






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