Distinct, specific IL-17- and IL-22-producing CD4+ T cell subsets contribute to the human anti-mycobacterial immune response

J Immunol. 2008 Feb 1;180(3):1962-70. doi: 10.4049/jimmunol.180.3.1962.

Abstract

We investigated whether the proinflammatory T cell cytokines IL-17 and IL-22 are induced by human mycobacterial infection. Remarkably, >20% of specific cytokine-producing CD4(+) T cells in peripheral blood of healthy, mycobacteria-exposed adults expressed IL-17 or IL-22. Specific IL-17- and IL-22-producing CD4(+) T cells were distinct from each other and from Th1 cytokine-producing cells. These cells had phenotypic characteristics of long-lived central memory cells. In patients with tuberculosis disease, peripheral blood frequencies of these cells were reduced, whereas bronchoalveolar lavage fluid contained higher levels of IL-22 protein compared with healthy controls. IL-17 was not detected in this fluid, which may be due to suppression by Th1 cytokines, as PBMC IL-17 production was inhibited by IFN-gamma in vitro. However, Th1 cytokines had no effect on IL-22 production in vitro. Our results imply that the magnitude and complexity of the anti-mycobacterial immune response have historically been underestimated. IL-17- and IL-22-producing CD4(+) T cells may play important roles in the human immune response to mycobacteria.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bronchoalveolar Lavage Fluid / immunology
  • CD4-Positive T-Lymphocytes / immunology*
  • Female
  • Humans
  • Immunologic Memory
  • Interleukin-17 / analysis
  • Interleukin-17 / metabolism*
  • Interleukin-22
  • Interleukins / analysis
  • Interleukins / metabolism*
  • Male
  • Mycobacterium tuberculosis / immunology*
  • T-Lymphocyte Subsets / immunology*
  • Th1 Cells / immunology
  • Tuberculosis, Pulmonary / immunology*

Substances

  • Interleukin-17
  • Interleukins