Studies with experimentally infected female mice have shown that gonococcal infection of the genital tract leads to the production of the inflammatory Th17-associated cytokines, IL-17 and IL-22, but not specific antibodies or cytokines typical of Th1- or Th2-driven adaptive immune responses, such as IFNγ or IL-4 (137, 162). This evidence concerns the gene IL17A and gonorrhea.