Innate type 1 immune response, but not IL-17 cells control tuberculosis infection.

The role of the innate immune response and host resistance to Mycobacterium tuberculosis infection (TB) is reviewed. Based on our data and the abundant literature, an early type 1 immune response is critical for infection control, while ILC3 and Th17 cells seem to be dispensable. Indeed, in M. tuberculosis infected mice, transcriptomic levels of Il17, Il17ra, Il22 and Il23a were not significantly modified as compared to controls, suggesting a limited role of IL-17 and IL-22 pathways in TB infection control. Neutralization of IL-17A or IL-17F did not affect infection control either. Ongoing clinical studies with IL-17 neutralizing antibodies show high efficacy in patients with psoriasis without increased incidence of TB infection or reactivation. Therefore, both experimental studies in mice and clinical trials in human patients suggest no risk of TB infection or reactivation by therapeutic IL-17 antibodies, unlike by TNF.