Role of IFN-γ in the establishment of anterior chamber-associated immune deviation (ACAID)-induced CD8+ T regulatory cells.
Introduction of alloantigens into the AC induces a form of immune tolerance known as ACAID, which induces antigen-specific CD8(+) Tregs, contributing to ocular immune privilege by down-regulating immune responses. Recent evidence suggests IFN-γ is needed for the suppressive function of CD8(+) ACAID Tregs. This study tested the hypothesis that IFN-γ is needed for alloantigen-specific ACAID CD8(+) Tregs to execute their suppressive function but is not required for the establishment of ACAID CD8(+) Tregs. To address this hypothesis, ACAID was induced by injecting BALB/c spleen cells into the AC of WT C57BL/6 mice, IFN-γ(-/-) C57BL/6 mice, or anti-IFN-γ-treated WT C57BL/6 mice. LAT assays using C57BL/6 APCs as stimulators, CD4(+) T cells from C57BL/6 mice previously immunized toward BALB/c alloantigens as effector cells, and IFN-γ-competent, IFN-γ(-/-), or IFN-γR(-/-) CD8(+) Tregs were used to evaluate the suppressive function of CD8(+) ACAID Tregs in response to IFN-γ. IFN-γ(-/-) mice or mice treated with anti-IFN-γ antibody prior to AC injection of alloantigen failed to develop ACAID. The suppressive function of IFN-γ(-/-) ACAID CD8(+) Tregs was restored through the administration of exogenous IFN-γ. This suppressive responsiveness toward IFN-γ was CD8(+) Treg-intrinsic, as CD8(+) Tregs from IFN-γR(-/-) mice, which were primed in the AC with alloantigens, were not able to suppress alloantigen-specific DTH responses. These results indicate that IFN-γ is not needed for the induction of CD8(+) ACAID Tregs but is required for ACAID Tregs to exert the suppression of allospecific DTH responses.[1]References
- Role of IFN-γ in the establishment of anterior chamber-associated immune deviation (ACAID)-induced CD8+ T regulatory cells. Paunicka, K., Chen, P.W., Niederkorn, J.Y. J. Leukoc. Biol. (2012) [Pubmed]
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