The data obtained from bacterial OVA-specific or TLR2-dependent colitis model utilizing NOD2-deficient and NOD2-transgenic mice provide evidence that the crosstalk between NOD2 and TLR2 contributes to the maintenance of intestinal homeostasis and that NOD2 functions as a negative regulator of TLR2-mediated colitogenic Th1 responses. The gene discussed is NOD2; the disease is colitis.