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The Journal of Immunology, 2006, 177: 8331-8337.
Copyright © 2006 by The American Association of Immunologists, Inc.

{gamma}{delta} T Cells Promote Anterior Chamber-Associated Immune Deviation and Immune Privilege through Their Production of IL-101

Hossam M. Ashour* and Jerry Y. Niederkorn2,{dagger}

* Immunology Graduate Program and {dagger} Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, TX 75390

Anterior chamber-associated immune deviation (ACAID) is a form of peripheral tolerance that is induced by introducing Ags into the anterior chamber (AC) of the eye, and is maintained by Ag-specific regulatory T cells (Tregs). ACAID regulates harmful immune responses that can lead to irreparable injury to innocent bystander cells that are incapable of regeneration. This form of immune privilege in the eye is mediated through Tregs and is a product of complex cellular interactions. These involve F4/80+ ocular APCs, B cells, NKT cells, CD4+CD25+ Tregs, and CD8+ Tregs. {gamma}{delta} T cells are crucial for the generation of ACAID and for corneal allograft survival. However, the functions of {gamma}{delta} T cells in ACAID are unknown. Several hypotheses were proposed for determining the functions of {gamma}{delta} T cells in ACAID. The results indicate that {gamma}{delta} T cells do not cause direct suppression of delayed-type hypersensitivity nor do they act as tolerogenic APCs. In contrast, {gamma}{delta} T cells were shown to secrete IL-10 and facilitate the generation of ACAID Tregs. Moreover, the contribution of {gamma}{delta} T cells ACAID generation could be replaced by adding exogenous recombinant mouse IL-10 to ACAID spleen cell cultures lacking {gamma}{delta} T cells.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

1 This work was supported by National Institutes of Health Grants EY005631 and EY016664 and an unrestricted grant from Research to Prevent Blindness, New York, NY.

2 Address correspondence and reprint requests to Dr. Jerry Y. Niederkorn, Department of Ophthalmology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390. E-mail address: jerry.niederkorn{at}utsouthwestern.edu

3 Abbreviations used in this paper used: ACAID, anterior chamber-associated immune deviation; AC, anterior chamber; Treg, T regulatory cell; DTH, delayed-type hypersensitivity; MHC-II, MHC class II; KO, knockout; rm recombinant mouse; LAT, local adoptive transfer assay.




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Implication for the CD94/NKG2A-Qa-1 system in the generation and function of ocular-induced splenic CD8+ regulatory T cells
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[Abstract] [Full Text] [PDF]




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