The potential of regulatory T cell-based therapies for alopecia areata

Cytotoxic T lymphocyte has been a concern for the etiopathogenesis of alopecia areata (AA), some recent evidence suggests that the regulatory T (T(reg)) cell deficiency is also a contributing factor. In the lesional scalp of AA, T(reg) cells residing in the follicles are impaired, leading to dysregu...

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Autores principales: Wan, Sheng, Xu, Wen, Xie, Bo, Guan, Cuiping, Song, Xiuzu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Immunology
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10186346/
https://www.ncbi.nlm.nih.gov/pubmed/37205097
http://dx.doi.org/10.3389/fimmu.2023.1111547
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author Wan, Sheng
Xu, Wen
Xie, Bo
Guan, Cuiping
Song, Xiuzu
author_facet Wan, Sheng
Xu, Wen
Xie, Bo
Guan, Cuiping
Song, Xiuzu
author_sort Wan, Sheng
collection PubMed
description Cytotoxic T lymphocyte has been a concern for the etiopathogenesis of alopecia areata (AA), some recent evidence suggests that the regulatory T (T(reg)) cell deficiency is also a contributing factor. In the lesional scalp of AA, T(reg) cells residing in the follicles are impaired, leading to dysregulated local immunity and hair follicle (HF) regeneration disorders. New strategies are emerging to modulate T(reg) cells’ number and function for autoimmune diseases. There is much interest to boost T(reg) cells in AA patients to suppress the abnormal autoimmunity of HF and stimulate hair regeneration. With few satisfactory therapeutic regimens available for AA, T(reg) cell-based therapies could be the way forward. Specifically, CAR-T(reg) cells and novel formulations of low-dose IL-2 are the alternatives.
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spelling pubmed-101863462023-05-17 The potential of regulatory T cell-based therapies for alopecia areata Wan, Sheng Xu, Wen Xie, Bo Guan, Cuiping Song, Xiuzu Front Immunol Immunology Cytotoxic T lymphocyte has been a concern for the etiopathogenesis of alopecia areata (AA), some recent evidence suggests that the regulatory T (T(reg)) cell deficiency is also a contributing factor. In the lesional scalp of AA, T(reg) cells residing in the follicles are impaired, leading to dysregulated local immunity and hair follicle (HF) regeneration disorders. New strategies are emerging to modulate T(reg) cells’ number and function for autoimmune diseases. There is much interest to boost T(reg) cells in AA patients to suppress the abnormal autoimmunity of HF and stimulate hair regeneration. With few satisfactory therapeutic regimens available for AA, T(reg) cell-based therapies could be the way forward. Specifically, CAR-T(reg) cells and novel formulations of low-dose IL-2 are the alternatives. Frontiers Media S.A. 2023-05-02 /pmc/articles/PMC10186346/ /pubmed/37205097 http://dx.doi.org/10.3389/fimmu.2023.1111547 Text en Copyright © 2023 Wan, Xu, Xie, Guan and Song https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Immunology
Wan, Sheng
Xu, Wen
Xie, Bo
Guan, Cuiping
Song, Xiuzu
The potential of regulatory T cell-based therapies for alopecia areata
title The potential of regulatory T cell-based therapies for alopecia areata
title_full The potential of regulatory T cell-based therapies for alopecia areata
title_fullStr The potential of regulatory T cell-based therapies for alopecia areata
title_full_unstemmed The potential of regulatory T cell-based therapies for alopecia areata
title_short The potential of regulatory T cell-based therapies for alopecia areata
title_sort potential of regulatory t cell-based therapies for alopecia areata
topic Immunology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10186346/
https://www.ncbi.nlm.nih.gov/pubmed/37205097
http://dx.doi.org/10.3389/fimmu.2023.1111547
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