Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?

Sun protection has been recommended by public health authorities to reduce the risk of keratinocyte and melanocyte tumors, yet some sun exposure is required for vitamin D synthesis. Frontal fibrosing alopecia (FFA) is a cicatricial alopecia that has been reported to have an association with facial p...

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Autor principal: Noakes, Rowland
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Hypothesis
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399449/
https://www.ncbi.nlm.nih.gov/pubmed/32801823
http://dx.doi.org/10.2147/CCID.S262803
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author Noakes, Rowland
author_facet Noakes, Rowland
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description Sun protection has been recommended by public health authorities to reduce the risk of keratinocyte and melanocyte tumors, yet some sun exposure is required for vitamin D synthesis. Frontal fibrosing alopecia (FFA) is a cicatricial alopecia that has been reported to have an association with facial photoprotection. The brief review proposes the hypothesis that FFA arises as a result of excessive facial photo-protection with a resultant disturbance in immunological homeostasis mediated via the aryl hydrocarbon receptor-kynurenine pathway axis (AHR/KP) leading to the collapse of immune privilege at the hair bulge.
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spelling pubmed-73994492020-08-14 Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin? Noakes, Rowland Clin Cosmet Investig Dermatol Hypothesis Sun protection has been recommended by public health authorities to reduce the risk of keratinocyte and melanocyte tumors, yet some sun exposure is required for vitamin D synthesis. Frontal fibrosing alopecia (FFA) is a cicatricial alopecia that has been reported to have an association with facial photoprotection. The brief review proposes the hypothesis that FFA arises as a result of excessive facial photo-protection with a resultant disturbance in immunological homeostasis mediated via the aryl hydrocarbon receptor-kynurenine pathway axis (AHR/KP) leading to the collapse of immune privilege at the hair bulge. Dove 2020-07-27 /pmc/articles/PMC7399449/ /pubmed/32801823 http://dx.doi.org/10.2147/CCID.S262803 Text en © 2020 Noakes. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Hypothesis
Noakes, Rowland
Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?
title Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?
title_full Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?
title_fullStr Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?
title_full_unstemmed Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?
title_short Frontal Fibrosing Alopecia. An Example of Disrupted Aryl Hydrocarbon Receptor-Mediated Immunological Homeostasis in the Skin?
title_sort frontal fibrosing alopecia. an example of disrupted aryl hydrocarbon receptor-mediated immunological homeostasis in the skin?
topic Hypothesis
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399449/
https://www.ncbi.nlm.nih.gov/pubmed/32801823
http://dx.doi.org/10.2147/CCID.S262803
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