Nevertheless, Toll-like receptor signaling had a trend of inhibition in the time period from the acute to chronic fasciolosis, suggesting that F. hepatica could somehow overcome and interfere in the downstream effect triggered by increased TLR2 and TLR4. The suppression of TLR4 and TLR functions by antigenic components such as one of the F. hepatica fatty acid binding proteins (58) and glycoconjugates (59) has previously been reported. The gene discussed is TLR4; the disease is fascioliasis.