Studies on TLR2, NLRP3, TLR5, and NODs did not evidence major species-specific responses, at least in responses to live bacteria, reinforcing the hypothesis that TLR4 plays a complex yet instrumental role in host specific responses to L. interrogans. However, we believe that the complexity of host specificities in leptospirosis results from the integration of several innate immune mechanisms, which may explain the vast diversity of leptospirosis diseases in different host species. This evidence concerns the gene TLR4 and leptospirosis.