Anti-inflammatory treatment of
autoimmune diseases is associated with an increased risk of reactivation
tuberculosis (TB). Besides
interleukin (IL-17)A,
IL-22 represents a classical T helper (TH)17
cytokine and shares similar pathological effects in inflammatory diseases such as
psoriasis or
arthritis. Whereas
IL-17A supports protective immune responses during mycobacterial
infections, the role of
IL-22 after
infection with Mycobacterium tuberculosis (Mtb) is yet poorly characterized. Therefore, we here characterize the cell types producing
IL-22 and the protective function of this
cytokine during experimental TB in mice. Like
IL-17A,
IL-22 is expressed early after
infection with Mtb in an IL-23-dependent manner. Surprisingly, the majority of IL-22-producing cells are not positive for
IL-17A but have rather functional characteristics of
interferon-gamma-producing TH1 cells. Although we found minor differences in the number of naive and central memory T cells as well as in the frequency of TH1 and polyfunctional T cells in mice deficient for
IL-22, the absence of
IL-22 does not affect the outcome of Mtb
infection. Our study revealed that although produced by TH1 cells,
IL-22 is dispensable for protective immune responses during TB. Therefore, targeting of
IL-22 in inflammatory disease may represent a therapeutic approach that does not incur the danger of reactivation TB.