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Immunity. 2015 Jul 21;43(1):107-19. doi: 10.1016/j.immuni.2015.06.009. Epub 2015 Jun 30.

Retinoic Acid Differentially Regulates the Migration of Innate Lymphoid Cell Subsets to the Gut.

Author information

1
Laboratory of Immunology and Hematopoiesis, Department of Comparative Pathobiology, Purdue Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA.
2
Department of Biological Sciences, Purdue University, West Lafayette, IN 47907, USA; Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA.
3
Laboratory of Immunology and Hematopoiesis, Department of Comparative Pathobiology, Purdue Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA; Center for Cancer Research, Purdue University, West Lafayette, IN 47907, USA; Weldon School of Biomedical Engineering, Purdue University, West Lafayette, IN 47907, USA. Electronic address: chkim@purdue.edu.

Abstract

Distinct 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.

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PMID:
26141583
PMCID:
PMC4511719
DOI:
10.1016/j.immuni.2015.06.009
[Indexed for MEDLINE]
Free PMC Article

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