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- W1543281625 abstract "Abstract Previous studies have demonstrated that activated Tregs express latent TGF-β1 on their cell surface bound to the tethering molecule GARP. Although integrins have been implicated in mediating the release of biologically active TGF-β1 from the complex of latent TGF-β1 and latent TGF-β1 binding protein, their role in processing latent TGF-β1 from the latent TGF-β1/GARP complex is unclear. We detected integrin β8 expression by CD4+Foxp3+ Treg, but not by CD4+Foxp3- T cells, by qRT-PCR. Furthermore, integrin β8 expression appeared to be a marker of thymically-derived Treg (tTreg), as its could not be detected on Foxp3+ T cells induced in vitro nor in vivo on peripherally induced Foxp3+Helios- Tregs. While Tregs from integrin β8 conditional knockouts suppressed T effector cell proliferation normally in vitro and in vivo in a model of colitis, integrin β8 deficient Tregs failed to provide a source of TGF-β1 to drive Th17 or iTreg differentiation in vitro. In addition, the knockout Tregs expressed higher levels of latent TGF-β1 on their cell surface consistent with defective processing. Taken together, integrin β8 is not only a marker of tTregs, but also functions in a cell intrinsic manner as the major pathway for processing latent TGF-β1 from the latent TGF-β1/GARP complex on the surface tTregs." @default.
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- W1543281625 date "2014-05-01" @default.
- W1543281625 modified "2023-09-23" @default.
- W1543281625 title "Integrin β8 is a marker of mouse regulatory T-cells (Treg) and is required for processing of latent TGF-β1 from the GARP/latent TGF-β1 complex. (IRC4P.483)" @default.
- W1543281625 doi "https://doi.org/10.4049/jimmunol.192.supp.60.10" @default.
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