Regulatory T Cells In Skin Facilitate Epithelial Stem Cell Differentiation.

alscarmuzza

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Authors:
Ali N; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA; Cutaneous Medicine Unit, St. John's Institute of Dermatology, King's College London, London WC2R 2LS, UK.
Zirak B; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Rodriguez RS; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Pauli ML; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Truong HA; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Lai K; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Ahn R; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Corbin K; Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Lowe MM; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Scharschmidt TC; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Taravati K; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Tan MR; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Ricardo-Gonzalez RR; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Nosbaum A; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Bertolini M; Department of Dermatology, University of Muenster, 48149 Muenster, Germany.
Liao W; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA.
Nestle FO; Cutaneous Medicine Unit, St. John's Institute of Dermatology, King's College London, London WC2R 2LS, UK.
Paus R; Centre for Dermatological Research, University of Manchester & NIHR Manchester Biomedical Research Centre, Manchester M13 9PL, UK.
Cotsarelis G; Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Abbas AK; Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.
Rosenblum MD; Department of Dermatology, University of California, San Francisco, San Francisco, CA 94143, USA. Electronic address: michael.rosenblum@ucsf.edu.
Source:
Cell [Cell] 2017 Jun 01; Vol. 169 (6), pp. 1119-1129.e11. Date of Electronic Publication: 2017 May 25.
Publication Type:
Journal Article
Language:
English
Journal Info:
Publisher: Cell Press Country of Publication: United States NLM ID: 0413066 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4172 (Electronic) Linking ISSN: 00928674 NLM ISO Abbreviation: Cell Subsets: MEDLINE


Abstract:
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 Tregsand 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.
 

cocona

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What we need now is a measure of tregs in the scalp of aa sufferers vs non-aa sufferers and see if there is a discrepancy. If A.A. is linked to a shortage of tregs in the scalp then that would suggest restoring tregs as a method of attacking A.A. with regenerative methods as well as explain in a bit more detail why even though non-aa sufferers follicles are constantly getting destroyed.(Via DHT based inflammation maybe?)

Just like A.A. sufferers the non-aa sufferers follicles still regenerate and stay active long term despite approximately equivalent levels of dht.

This would weaken the whole follicles on the top of your head are dht sensitive hypothesis and replace it with aa causes a shortage of tregs in the top of the scalp which impairs said follicles ability to regenerate.

Don't mind my armchair cellular biology.==
 
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