Retinoic Acid Differentially Regulates the Migration of Innate Lymphoid Cell Subsets to the Gut
| Autor: | Chang H. Kim, Elizabeth J. Taparowsky, Myung H. Kim |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Receptors
CCR7 Population Immunology Retinoic acid Tretinoin Biology Mice Receptors CCR 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Cell Movement Animals Immunology and Allergy Intestinal Mucosa education Receptor skin and connective tissue diseases Cells Cultured 030304 developmental biology Mice Knockout 0303 health sciences education.field_of_study Innate immune system Innate lymphoid cell Enterobacteriaceae Infections Dendritic Cells Immunity Innate Lymphocyte Subsets Gut-specific homing Cell biology Intestines Mice Inbred C57BL body regions Infectious Diseases chemistry Tissue tropism Citrobacter rodentium 030215 immunology Homing (hematopoietic) |
| Zdroj: | Immunity. 43(1):107-119 |
| ISSN: | 1074-7613 |
| DOI: | 10.1016/j.immuni.2015.06.009 |
| Popis: | SummaryDistinct groups of innate lymphoid cells (ILCs) such as ILC1, ILC2, and ILC3 populate the intestine, but how these ILCs develop tissue tropism for this organ is unclear. We report that prior to migration to the intestine ILCs first undergo a “switch” in their expression of homing receptors from lymphoid to gut homing receptors. This process is regulated by mucosal dendritic cells and the gut-specific tissue factor retinoic acid (RA). This change in homing receptors is required for long-term population and effector function of ILCs in the intestine. Only ILC1 and ILC3, but not ILC2, undergo the RA-dependent homing receptor switch in gut-associated lymphoid tissues. In contrast, ILC2 acquire gut homing receptors in a largely RA-independent manner during their development in the bone marrow and can migrate directly to the intestine. Thus, distinct programs regulate the migration of ILC subsets to the intestine for regulation of innate immunity. |
| Databáze: | OpenAIRE |
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