Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria.
Immunity, 2012/12/14;37(6):1061-75.
Basu R[1], O'Quinn DB, Silberger DJ, Schoeb TR, Fouser L, Ouyang W, Hatton RD, Weaver CT
Affiliations
PMID: 23200827
Impact factor: 43.474
Abstract
Interleukin-22 (IL-22) is central to host protection against bacterial infections at barrier sites. Both innate lymphoid cells (ILCs) and T cells produce IL-22. However, the specific contributions of CD4(+) T cells and their developmental origins are unclear. We found that the enteric pathogen Citrobacter rodentium induced sequential waves of IL-22-producing ILCs and CD4(+) T cells that were each critical to host defense during a primary infection. Whereas IL-22 production by ILCs was strictly IL-23 dependent, development of IL-22-producing CD4(+) T cells occurred via an IL-6-dependent mechanism that was augmented by, but not dependent on, IL-23 and was dependent on both transcription factors T-bet and AhR. Transfer of CD4(+) T cells differentiated with IL-6 in the absence of TGF-β ("Th22" cells) conferred complete protection of infected IL-22-deficient mice whereas transferred Th17 cells did not. These findings establish Th22 cells as an important component of mucosal antimicrobial host defense.
MeSH terms
Animals; Citrobacter rodentium; Enterobacteriaceae Infections; Gene Expression Regulation; Inflammation Mediators; Interleukin-23; Interleukin-6; Interleukins; Mice; Mice, Knockout; Mucous Membrane; Nuclear Receptor Subfamily 1, Group F, Member 3; Receptors, Aryl Hydrocarbon; T-Box Domain Proteins; T-Lymphocytes, Helper-Inducer; Th17 Cells; Interleukin-22
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