IL17A and tuberculosis: Contrary to the debatable PGL hypervirulence effects where M. tuberculosis PGL-deficient strains induce pro-inflammation (141), recent studies, using a necrotic M. tuberculosis mouse model, show that loss of M. tuberculosis PGLs decreases the Th17 response (e.g., IL-17A), where IL-17A production seems critical to limit the development of hypoxic necrotic granulomas and reduces disease severity in TB (142).