In addition to TLR4, other TLRs have been shown to play a role in the pathogenesis of intestinal inflammation, poten-tially via TLR-dependent signaling of the enterocytes themselves. For instance, both TLR2-/-and TLR9-/-mice were found recently to develop more severe intestinal inflammation compared with wild-type counterparts (90, 91) . Moreover, TLR5-/-mice have been found to develop spontaneous colitis (92) and the TLR5 ligand flagellin has been found to protect against enterocyte apoptosis (93) . These findings indicate that TLR2, TLR5, and TLR9 may exert protective roles in the pathogenesis of intestinal inflammation, or indeed may provide support for the maintenance of intestinal homeostasis. Since TLR2, TLR5, and TLR9 share the downstream mediator MyD88, it is possible that these studies provide mechanistic insights into the protective role of MyD88 in the maintenance of intestinal homeostasis as identified by Medzhitov et al. (83) . Once again, though the story is more complicated than appears on first glance, as activation of TLR3, the only TLR family member that does not require MyD88 to signal, with the specific ligand polyinosinic:polycytidylic acid (poly I:C) protected against the severity of DSS-induced colitis (94) .