| Background |
Integrin α5β8 facilitates activation and release of TGF-β, which has immunosuppressive effects Deletion of integrin β8 from dendritic cells led to development of inflammatory bowl disease and autoimmunity in mice, as well as failure to induce regulatory T cells that require TGF-β for development TGF-β is also involved in Th17 cell differentiation. Mice lacking expression of integrin β8 on dendritic cells fail to develop Th17 cells and are protected from Th17-mediated autoimmune disease Regulatory T cells express high levels of integrin α5β8, which enables them to suppress pathogenic T cell activation by activating latent TGF-β Integrin β8 is also essential for vascular morphogenesis as integrin β8-deficient mice are embryonic or perinatal lethal and exhibit insufficient and abnormal vascular morphogenesis.
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