Mycobacterium tuberculosis suppresses protective Th17 responses during infection.

Mycobacterium tuberculosis suppresses IL-17A-producing Th17 responses during primary mouse infection, and ESX-1 and PDIM mutants show significantly increased Th17 cells and IL-17A in lungs.

• Why it matters: Protective Th17 development correlates with human protection, but Th17s are rare in primary infection; the mechanisms by which M. tuberculosis prevents consistent Th17 induction were unknown.
• What they did: The study tested whether Th17 absence depends on infection route or duration, then used Tbx21-deficient mice and ESX-1 and PDIM mutant infections, measuring Th17/IL-17A and IL-23 in dendritic cells.
• The result: Th17 suppression is IFN-γ-independent and independent of type I IFN, but ESX-1 and PDIM reduce IL-23 production in mediastinal lymph node dendritic cells, and IL-17A deficiency partially restores virulence of ESX-1 and PDIM mutants.