IL17A and infection: In addition, the magnitude of the Th17 response was found to be important, since mice repeatedly exposed to MTb and BCG developed strong IL-23-induced Th17 cell responses that became pathogenic rather than protective, with an IL-17/macrophage inflammatory protein-2- (MIP-2-) dependent influx of neutrophils and induction of lung pathology rather than containment of infection [30].