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- W4313386145 abstract "Abstract Regulatory T (Treg) cells are essential for self tolerance and immune homeostasis, which is subjected to regulation by multiple molecular switches. gp96/grp94 is an endoplasmic reticulum (ER) resident chaperone, and it plays an important immune regulatory function by folding Toll-like receptors and integrins. In this study, we demonstrated that gp96 is critically required for immune suppressive function of Treg cells. Disruption of gp96 in mice through Treg-specific gp96 knockout (KO) leads to impairment of suppressive function of Treg cells in vivo and development of fatal inflammatory diseases. Mechanistically, we found that Treg cells showed lineage instability in the absence of gp96, and underwent conversion to IFN-γ producing pathogenic T cells. Moreover, we unveiled that GARP, a cell surface docking receptor for latent membrane-associated TGF-b (mLTGF-b), is the client protein of gp96. The dual loss of GARP and integrins renders gp96 KO Treg cells incapable of expressing mLTGF-b and inefficient in producing active TGF-b. In the B16 tumor bearing mice, transient and inducible depletion of gp96 in Treg cells robustly improved therapeutic efficacy of adoptively transferred gp100-specific CD8 T cells without causing auto-inflammatory diseases. In summary, our study demonstrates that gp96 regulates multiple facets of Treg cell biology, and it suggests a manipulation of gp96 expression in Treg cells as a promising strategy to enhance cancer immunotherapy." @default.
- W4313386145 created "2023-01-06" @default.
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- W4313386145 date "2015-05-01" @default.
- W4313386145 modified "2023-09-25" @default.
- W4313386145 title "Molecular chaperone gp96/grp94 is critical for immunosuppressive functions of regulatory T cells (IRM15P.458)" @default.
- W4313386145 doi "https://doi.org/10.4049/jimmunol.194.supp.199.6" @default.
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