Interestingly, although only γδ T-IEL secrete KGF, both CD100−/− colonic γδ and αβ T-IEL were shown to have defective proliferative capacity following DSS-induced colitis.77 However, plexin B2-CD100 interactions did not play a role in αβ T cell activation in vitro,81 suggesting that while CD100 is highly expressed on all T cells, it functions in a subset- and site-specific manner, perhaps depending on the type of ligand expressed. This evidence concerns the gene SEMA4D and colitis.