{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Paunicka K"],"funding":["NEI NIH HHS","Research to Prevent Blindness","NIH"],"pagination":["475-83"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3289396"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["91(3)"],"pubmed_abstract":["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 "],"journal":["Journal of leukocyte biology"],"pubmed_title":["Role of IFN-γ in the establishment of anterior chamber-associated immune deviation (ACAID)-induced CD8+ T regulatory cells."],"pmcid":["PMC3289396"],"funding_grant_id":["P30 EY020799","EY005631","EY 020799","R01 EY005631","EY020799"],"pubmed_authors":["Chen PW","Niederkorn JY","Paunicka K"],"additional_accession":[]},"is_claimable":false,"name":"Role of IFN-γ in the establishment of anterior chamber-associated immune deviation (ACAID)-induced CD8+ T regulatory cells.","description":"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 ","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012 Mar","modification":"2026-05-03T05:52:22.098Z","creation":"2019-03-27T00:49:35Z"},"accession":"S-EPMC3289396","cross_references":{"pubmed":["22180630"],"doi":["10.1189/jlb.0311173"]}}