Effect of human corneal resident cells on the immune modulation of CD4 T cells (49.19)

Abstract Fibroblasts which are terminally differentiated stromal cells have been reported to share immunosuppressive effect on the lymphocyte activation with mesenchymal stem cells. However, the immunomodulatory role of the corneal residential stromal cells(keratocytes) have not been known. We inves...

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Published inThe Journal of immunology (1950) Vol. 188; no. 1_Supplement; pp. 49 - 49.19
Main Authors Ryu, Jin Suk, Jeong, Hyun Jeong, Lee, Young Eun, Kim, Mee Kum, Wee, Won Ryang
Format Journal Article
LanguageEnglish
Published 01.05.2012
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Summary:Abstract Fibroblasts which are terminally differentiated stromal cells have been reported to share immunosuppressive effect on the lymphocyte activation with mesenchymal stem cells. However, the immunomodulatory role of the corneal residential stromal cells(keratocytes) have not been known. We investigated the immunomodulatory effect of human keratocytes on the CD4+ T cells as a part of ocular immune privilege. The study was performed in accordance with the guidelines of the Declaration of Helsinki. Human peripheral blood mononuclear cells were obtained from the healthy voluntary donors with informed consents. CD4+ T cells were purified through MACS separator with the human CD4+ T Cell Isolation Kit II (Miltenyi Biotec). The human keratocytes were collected from the remaining donor graft. CFSE stained CD4+ T cells were stimulated with anti-CD3/CD28, and were then co-cultured with keratocytes with or without 1-methyltryptophan. The proliferation of T cells and the secretion of IFN-γ were evaluated. Changes of cytokine expression were also evaluated using ELISA after co-culture. We found that keratocytes suppressed the proliferation and the secretion of IFN-γ of CD4 T cells, and enhanced IL-10 and TGF-β, which were partially reversed with 1-methyltryptophan treatment. It implied that human keratocytes might have an immune modulatory effect on the CD4 T cells through indoleamine 2,3 dioxygenase-dependent in part, which seemed likely to contribute to ocular immune privilege.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.188.Supp.49.19