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International Immunology Advance Access originally published online on March 18, 2005
International Immunology 2005 17(5):523-530; doi:10.1093/intimm/dxh234
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© The Japanese Society for Immunology. 2005. All rights reserved. For permissions, please e-mail: journals.permissions@oupjournals.org

Critical contribution of CD80 and CD86 to induction of anterior chamber-associated immune deviation

Rintaro Tsukahara1,2, Masaru Takeuchi1, Hisaya Akiba2, Takeshi Kezuka1, Kazuyoshi Takeda2, Yoshihiko Usui1, Masahiko Usui1, Hideo Yagita2 and Ko Okumura2

1 Department of Ophthalmology, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan
2 Department of Immunology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan

Correspondence to: R. Tsukahara; E-mail: rintaro{at}tokyo-med.ac.jp

Intraocular inoculation of antigens induces anterior chamber-associated immune deviation (ACAID), which is mediated by development of regulatory T cells in response to antigen-presenting cells (APC) pre-conditioned by intraocular transforming growth factor-ß (TGF-ß). In this study, we examined the involvement of T-cell co-stimulatory molecules in this process. To mimic the intraocular APC, thioglycollate-elicited peritoneal exudate cells (PEC) were pre-treated with TGF-ß in vitro. Expression of CD80, CD86, OX40 ligand (OX40L) and CD70 was analyzed by flow cytometry. Contribution of these molecules to co-stimulatory activity of TGF-ß-treated PEC on antigen-stimulated T-cell proliferation and cytokine production was determined by inhibition with blocking antibodies in vitro. Contribution of CD80 and CD86 to induction of ACAID was determined by the administration of blocking antibodies at intraocular antigen inoculation in vivo. TGF-ß-treated PEC expressed CD80 and CD86 but not OX40L or CD70. Antigen-stimulated T cells proliferated and produced IL-10, but not IFN-{gamma}, in response to co-stimulation by TGF-ß-treated PEC, which was abrogated by blocking antibodies against CD80 and CD86. Induction of regulatory cells mediating ACAID was abolished by in vivo blockade of CD80 and CD86. The present results indicated that CD80 and CD86 play a critical role in induction of ACAID, possibly by co-stimulating expansion and IL-10 production of regulatory T cells in response to TGF-ß-conditioned APC.

Keywords: anterior chamber-associated immune deviation (ACAID), co-stimulatory molecules, regulatory T cells

Transmitting editor: K. Yamamoto


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