For example, isogenic mouse lines lacking the endotoxin receptor, Toll-like receptor 4 (TLR4), have a substantially higher burden of N. gonorrhoeae than do wild-type controls after vaginal infection, and this correlates with an exaggerated classical (TNF, CXCL1/KC, and CXCL2/MIP-2) inflammatory response but a diminished IL-17 response in TLR4-deficient mice (136–138). The gene discussed is CXCL2; the disease is infective vaginitis.