Consistent with this, we found that TLR2 expression was critical for the anti-colitogenic activity of Hsp65-LL, since TLR2−/− mice as well as mice deficient for the TLR2 adaptor molecules MyD88 and MAL/TIRAP, which mediate TLR2 signaling pathway (60), showed no improvement of colitis by the pretreatment of Hsp65-L. The gene discussed is MAL; the disease is colitis.