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Cell. 2019 Feb 21;176(5):982-997.e16. doi: 10.1016/j.cell.2018.12.031. Epub 2019 Jan 31.

Homeostatic Control of Sebaceous Glands by Innate Lymphoid Cells Regulates Commensal Bacteria Equilibrium.

Author information

1
Cutaneous Leukocyte Biology Section, Dermatology Branch, NIAMS, NIH, Bethesda, MD 20892, USA.
2
Cutaneous Leukocyte Biology Section, Dermatology Branch, NIAMS, NIH, Bethesda, MD 20892, USA; Department of Dermatology and Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea.
3
Cutaneous Microbiome and Inflammation Section, Dermatology Branch, NIAMS, NIH, Bethesda, MD 20892, USA.
4
Laboratory of Immunology, Molecular Immunology and Inflammation Branch, NIAMS, NIH, Bethesda, MD 20892, USA.
5
Human Genetics Section, Laboratory of Genetics and Genomics, NIA, NIH, Baltimore, MD 21224, USA.
6
Laboratory for Innate Immune Systems, RIKEN Center for Integrative Medical Sciences, Yokohama, 230-0045, Japan.
7
Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 113-8654, Japan.
8
Department of Orthopedic Surgery, National Defense Medical College, Tokorozawa, 359-8513, Japan.
9
Molecular and Cellular Immunoregulation Section, Laboratory of Immune System Biology, NIAID, NIH, Bethesda, MD 20892, USA.
10
Laboratory of Molecular Immunology and Immunology Center, NHLBI, NIH, Bethesda, MD 20892, USA.
11
Cutaneous Leukocyte Biology Section, Dermatology Branch, NIAMS, NIH, Bethesda, MD 20892, USA. Electronic address: keisuke.nagao@nih.gov.

Abstract

Immune cells and epithelium form sophisticated barrier systems in symbiotic relationships with microbiota. Evidence suggests that immune cells can sense microbes through intact barriers, but regulation of microbial commensalism remain largely unexplored. Here, we uncovered spatial compartmentalization of skin-resident innate lymphoid cells (ILCs) and modulation of sebaceous glands by a subset of RORγt+ ILCs residing within hair follicles in close proximity to sebaceous glands. Their persistence in skin required IL-7 and thymic stromal lymphopoietin, and localization was dependent on the chemokine receptor CCR6. ILC subsets expressed TNF receptor ligands, which limited sebocyte growth by repressing Notch signaling pathway. Consequently, loss of ILCs resulted in sebaceous hyperplasia with increased production of antimicrobial lipids and restricted commensalism of Gram-positive bacterial communities. Thus, epithelia-derived signals maintain skin-resident ILCs that regulate microbial commensalism through sebaceous gland-mediated tuning of the barrier surface, highlighting an immune-epithelia circuitry that facilitates host-microbe symbiosis.

PMID:
30712873
PMCID:
PMC6532063
[Available on 2019-08-21]
DOI:
10.1016/j.cell.2018.12.031

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