Transcription profiling of primed, ILT3-Fc treated CD8+ T suppressor cells vs. primed, untreated CD8+ counterparts
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE23922 | GEO | 2010/09/02
SECONDARY ACCESSION(S): PRJNA130509
REPOSITORIES: GEO
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Project description:CD3 T cells were first primed for 7 days with allogeneic APC in the presence of absence of ILT3-Fc, then were restimulated for 4 hours (with the original priming APC) CD8 T cells were magnetically sorted from these cultures, and lysed for gene chip profiling. Two condition experiments, ILT3Fc treated vs untreated CD8+ T cells, (4) ILT3Fc treated replicates and (4) untreated replicates
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Project description:Naïve T cell activation involves at least two signals from an antigen presenting cell (APC), one through the T cell receptor via interaction with APC peptide-MHC complexes and a second through interaction of CD28 with APC B7 ligands. Following activation, T cells up-regulate a host of other membrane-bound costimulatory molecules which can either promote or inhibit further T cell maturation and proliferation. In some cases, it is necessary to attenuate T cell activation to prevent deleterious inflammation, and inhibitory members of the B7/Butyrophilin family of ligands have evolved to balance the strong stimuli the activating B7 ligands confer. Human genetic association and in vitro studies have implicated one such ligand, BTNL2, in controlling inflammation at mucosal surfaces. Here we show that recombinant mouse BTNL2 modifies B7/CD28 signaling to promote expression of Foxp3, a transcription factor necessary for murine Treg development and function. BTNL2 blocks Akt-mediated inactivation of Foxo1, a transcription factor necessary for Foxp3 expression. Immunophenotyping and gene profiling reveal that BTNL2-induced Treg share many properties with natural Treg, and in vivo they suppress enteritis induced by mouse effector T cells. These findings describe a mechanism by which environmental antigen-driven formation of Treg may be orchestrated by APC expressing specific modulators of costimulatory signals.
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