期刊
JOURNAL OF IMMUNOLOGY
卷 196, 期 11, 页码 4731-4738出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1502673
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资金
- Institut Pasteur
- INSERM
- French government
- Ligue Nationale contre le Cancer
- Ligue Nationale contre le Cancer as an Equipe Labelisee
Group 3 innate lymphoid cells (ILC3) actively participate in mucosal defense and homeostasis through prompt secretion of IL-17A, IL-22, and IFN-gamma. Reports identify two ILC3 lineages: a CCR6(+)T-bet(-) subset that appears early in embryonic development and promotes lymphoid organogenesis and a CCR6(-)T-bet(+) subset that emerges after microbial colonization and harbors NKp46(+) ILC3. We demonstrate that NKp46 expression in the ILC3 subset is highly unstable. Cell fate mapping using Ncr1(CreGFP) x Rosa26(RFP) mice revealed the existence of an intestinal RFP+ ILC3 subset (Ncr1(FM)) lacking NKp46 expression at the transcript and protein levels. Ncr1(FM) ILC3 produced more IL-22 and were distinguishable from NKp46(+) ILC3 by differential CD117, CD49a, DNAX accessory molecule-1, and, surprisingly, CCR6 expression. Ncr1(FM) ILC3 emerged after birth and persisted in adult mice following broad-spectrum antibiotic treatment. These results identify an unexpected phenotypic instability within NKp46(+) ILC3 that suggests a major role for environmental signals in tuning ILC3 functional plasticity.
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