However, TGF-β2 does not contain the RGD integrin binding motif that would allow engagement with integrin αvβ8 and Ltbp-3 and tPA−/− mice do not develop signs of colitis akin to mice lacking αvβ8 on DCs.9,21 Therefore although CD103+ intestinal DCs express an abundance of factors involved in TGF-β availability, our data clearly show that αvβ8-mediated TGF-β activation is the critical activator of TGF-β responsible for enhanced Treg induction in the intestine. This evidence concerns the gene LTBP3 and colitis.