| First Author | Dumoutier L | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 4 | Pages | 1075-85 |
| PubMed ID | 21400499 | Mgi Jnum | J:175417 |
| Mgi Id | MGI:5285501 | Doi | 10.1002/eji.201040878 |
| Citation | Dumoutier L, et al. (2011) IL-22 is produced by gammaC-independent CD25+ CCR6+ innate murine spleen cells upon inflammatory stimuli and contributes to LPS-induced lethality. Eur J Immunol 41(4):1075-85 |
| abstractText | IL-22 is a Th17 cytokine that plays a key role in immune responses against extracellular bacteria. In mucosal lymphoid tissues, IL-22 production is mainly due to an IL-23-responsive NK-like cell subset that shares some markers with lymphoid tissue inducer (LTi) cells. Here, we identified a new spleen cell population responsible for IL-22 production upon either in vitro stimulation by anti-CD3 antibodies or in vivo stimulation by lipopolysaccharide (LPS) via IL-2- and an IL-23-dependent mechanisms, respectively. These cells represent 1% of spleen cells from recombination activating gene (Rag2)-deficient mice, and correspond to a discrete innate lymphoid cell population expressing CD25, CCR6 and IL-7R. This population comprises 60-70% CD4(+) cells, which produce IL-22, and are still present in common gamma chain-deficient mice; the CD4(-) subset coexpresses IL-22 and IL-17, and is common gamma chain-dependent. The importance of IL-22 production for the LPS-triggered response is highlighted by the fact that IL-22-deficient mice are more resistant to LPS-induced mortality. |
