Phenotypic and Functional Plasticity of Murine Intestinal NKp46+ Group 3 Innate Lymphoid Cells

Group 3 innate lymphoid cells (ILC3) actively participate in mucosal defense and homeostasis through prompt secretion of IL-17A, IL-22, and IFN-γ. Reports identify two ILC3 lineages: a CCR6(+)T-bet(-) subset that appears early in embryonic development and promotes lymphoid organogenesis and a CCR6(-...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2016-06, Vol.196 (11), p.4731-4738
Main Authors: Verrier, Thomas, Satoh-Takayama, Naoko, Serafini, Nicolas, Marie, Solenne, Di Santo, James P, Vosshenrich, Christian A J
Format: Article
Language:English
Subjects:
Animals
Antigens, Ly - immunology
Cells, Cultured
Immunity, Innate - immunology
Immunology
Innate immunity
Intestines - cytology
Intestines - immunology
Life Sciences
Lymphocytes - cytology
Lymphocytes - immunology
Mice
Mice, Transgenic
Natural Cytotoxicity Triggering Receptor 1 - immunology
Phenotype
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Summary:Group 3 innate lymphoid cells (ILC3) actively participate in mucosal defense and homeostasis through prompt secretion of IL-17A, IL-22, and IFN-γ. 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) × 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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1502673