Regulatory T cells in Skin Facilitate Epithelial Stem Cell Differentiation

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Summary

The maintenance of tissue homeostasis is critically dependent on the function of tissue-resident immune cells and the differentiation capacity of tissue-resident stem cells (SCs). How immune cells influence the function of SCs is largely unknown. Regulatory T cells (Tregs) in skin preferentially localize to hair follicles (HFs), which house a major subset of skin SCs (HFSCs). Here, we mechanistically dissect the role of Tregs in HF and HFSC biology. Lineage-specific cell depletion revealed that Tregs promote HF regeneration by augmenting HFSC proliferation and differentiation. Transcriptional and phenotypic profiling of T _regs and HFSCs revealed that skin-resident Tregs preferentially express high levels of the Notch ligand family member, Jagged 1 (Jag1). Expression of Jag1 on Tregs facilitated HFSC function and efficient HF regeneration. Taken together, our work demonstrates that Tregs in skin play a major role in HF biology by promoting the function of HFSCs.

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Label-retaining cells reside in the bulge area of pilosebaceous unit: implications for follicular stem cells, hair cycle, and skin carcinogenesis.

George Cotsarelis, Tung-Tien Sun, Robert Lavker (1990)

Inconsistent with the view that hair follicle stem cells reside in the matrix area of the hair bulb, we found that label-retaining cells exist exclusively in the bulge area of the mouse hair follicle. The bulge consists of a subpopulation of outer root sheath cells located in the midportion of the follicle at the arrector pili muscle attachment site. Keratinocytes in the bulge area are relatively undifferentiated ultrastructurally. They are normally slow cycling, but can be stimulated to proliferate transiently by TPA. Located in a well-protected and nourished environment, these cells mark the lower end of the "permanent" portion of the follicle. Our findings, plus a reevaluation of the literature, suggest that follicular stem cells reside in the bulge region, instead of the lower bulb. This new view provides insights into hair cycle control and the possible involvement of hair follicle stem cells in skin carcinogenesis.

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Epidermal homeostasis: a balancing act of stem cells in the skin.

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The skin epidermis and its array of appendages undergo ongoing renewal by a process called homeostasis. Stem cells in the epidermis have a crucial role in maintaining tissue homeostasis by providing new cells to replace those that are constantly lost during tissue turnover or following injury. Different resident skin stem cell pools contribute to the maintenance and repair of the various epidermal tissues of the skin, including interfollicular epidermis, hair follicles and sebaceous glands. Interestingly, the basic mechanisms and signalling pathways that orchestrate epithelial morphogenesis in the skin are reused during adult life to regulate skin homeostasis.

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Genome-wide association study in alopecia areata implicates both innate and adaptive immunity.

Lynn Petukhova, Madeleine Duvic, Maria Hordinsky … (2010)

Alopecia areata (AA) is among the most highly prevalent human autoimmune diseases, leading to disfiguring hair loss due to the collapse of immune privilege of the hair follicle and subsequent autoimmune attack. The genetic basis of AA is largely unknown. We undertook a genome-wide association study (GWAS) in a sample of 1,054 cases and 3,278 controls and identified 139 single nucleotide polymorphisms that are significantly associated with AA (P

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Author and article information

Journal

Journal ID (nlm-journal-id): 0413066

Journal ID (pubmed-jr-id): 2830

Journal ID (nlm-ta): Cell

Journal ID (iso-abbrev): Cell

Title: Cell

ISSN (Print): 0092-8674

ISSN (Electronic): 1097-4172

Publication date Nihms-submitted: 10 May 2017

Publication date (Electronic): 25 May 2017

Publication date (Print): 01 June 2017

Publication date PMC-release: 01 June 2018

Volume: 169

Issue: 6

Pages: 1119-1129.e11

Affiliations

[1 ]Department of Dermatology, UCSF, San Francisco, California, USA

[2 ]Department of Pathology, UCSF, San Francisco, California, USA

[3 ]Cutaneous Medicine Unit, St. John’s Institute of Dermatology, King’s College London, London, UK

[4 ]Department of Dermatology, University of Muenster, Muenster, Germany

[5 ]Centre for Dermatological Research, University of Manchester & NIHR Manchester Biomedical Research Centre, Manchester, UK

[6 ]Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA

Author notes

Corresponding author: Michael D. Rosenblum, Michael.Rosenblum@ 123456ucsf.edu , Phone number: +1 415.476.1685, Fax number: +1 415.502.3334

[7]

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Article

Accession ID: PMC5504703 Pmcid ID: PMC5504703 Pmc-uid ID: 5504703 Manuscript ID: nihpa873913

DOI: 10.1016/j.cell.2017.05.002

PMC ID: 5504703

PubMed ID: 28552347

SO-VID: 371a3903-265d-4b0d-bf1c-ccd55767fbed

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