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IL-22 is mainly produced by IFNγ-secreting cells but is dispensable for host protection against Mycobacterium tuberculosis infection.

Abstract
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.
AuthorsJochen Behrends, Jean-Christophe Renauld, Stefan Ehlers, Christoph Hölscher
JournalPloS one (PLoS One) Vol. 8 Issue 2 Pg. e57379 ( 2013) ISSN: 1932-6203 [Electronic] United States
PMID23460846 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Antigens, Bacterial
  • Inflammation Mediators
  • Interleukin-23
  • Interleukins
  • Interferon-gamma
  • interleukin-22
Topics
  • Animals
  • Antigens, Bacterial (immunology)
  • CD4-Positive T-Lymphocytes (immunology)
  • Granulocytes (metabolism)
  • Host-Pathogen Interactions (immunology)
  • Immunity (immunology)
  • Inflammation Mediators (metabolism)
  • Interferon-gamma (biosynthesis, metabolism)
  • Interleukin-23 (metabolism)
  • Interleukins (biosynthesis, deficiency)
  • Lymphocyte Activation (immunology)
  • Macrophage Activation (immunology)
  • Macrophages (metabolism, microbiology)
  • Mice
  • Mice, Inbred C57BL
  • Mycobacterium tuberculosis (physiology)
  • Th1 Cells (immunology)
  • Th17 Cells (immunology)
  • Tuberculosis (immunology, microbiology, prevention & control)

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