Local secretion of stress hormones increases in alopecia areata lesions after treatment with UVA‐1 phototherapy

Cuéllar-Barboza, Adrián; Garza, Jesús Alberto Cárdenas‐de la; Cruz-Gomez, Luis Gerardo; Barboza-Quintana, Oralia; Flores‐Gutiérrez, Juan Pablo; Gómez‐Flores, Minerva; Welsh, Oliverio; Ocampo‐Candiani, Jorge; Herz‐Ruelas, Maira Elizabeth

doi:10.1111/exd.14077

Cited by 10 publications

(9 citation statements)

References 19 publications

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“…There is also some evidence that current therapies indirectly facilitate HF IP restoration. For example, the potent IP guardian, αMSH, increases when AA is treated with UVA‐1 phototherapy 329 . Diphencyprone (DCP) treatment normalizes MHC expression in HFs and promotes IL‐10 and TGFβ1 expression 330‐332 .…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

182

157

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Anagen stage hair follicles (HFs) exhibit “immune privilege (IP)” from the level of the bulge downwards to the bulb. Both passive and active IP mechanisms protect HFs from physiologically undesired immune responses and limit immune surveillance. IP is relative, not absolute, and is primarily based on absent, or greatly reduced, intra‐follicular antigen presentation via MHC class I and II molecules, along with prominent expression of “no danger” signals like CD200 and the creation of an immunoinhibitory signalling milieu generated by the secretory activities of HFs. Perifollicular mast cells, Tregs and other immunocytes may also contribute to HF IP maintenance in healthy human skin. Collapse of anagen hair bulb IP is an essential prerequisite for the development of alopecia areata (AA). In AA, lesional HFs are rapidly infiltrated by NKG2D + T cells and natural killer (NK) cells, while perifollicular mast cells acquire a profoundly pro‐inflammatory phenotype and interact with autoreactive CD8+ T cells. Using animal models, significant functional evidence has accumulated that demonstrates the dominance of the immune system in AA pathogenesis. Purified CD8+T‐cell and NK cell populations alone, which secrete fγ, suffice to induce the AA phenotype, while CD4+T‐cells aggravate it, and Tregs and iNKT cells may provide relative protection against AA development. While IP collapse may be induced by exogenous agents, inherent IP deficiencies might confer increased susceptibility to AA for some individuals. Thus, a key goal for effective AA management is the re‐establishment of a functional HF IP, which will also provide superior protection from disease relapse.

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Section: Therapeutic Perspectivesmentioning

confidence: 99%

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

182

157

View full text Add to dashboard Cite

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“…101 Notably, the primary impact of CRH is pro-inflammatory, and an anti-inflammatory impact is the secondary effect of ACTH and α-MSH. 105 Among the various POMC peptides, ACTH is considered to exert the most profound influence on the growth of hair. MC2R is a member of the G protein-coupled receptor superfamily, which belongs to the melanocortin receptor family.…”

Section: Rel Ati Ons Hip B E T Ween Neurog Eni C Infl Ammati On the ...mentioning

confidence: 99%

Role of neurogenic inflammation in the pathogenesis of alopecia areata

Shi,

Wan,

Song

2024

The Journal of Dermatology

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Alopecia areata refers to an autoimmune illness indicated by persistent inflammation. The key requirement for alopecia areata occurrence is the disruption of immune‐privileged regions within the hair follicles. Recent research has indicated that neuropeptides play a role in the damage to hair follicles by triggering neurogenic inflammation, stimulating mast cells ambient the follicles, and promoting apoptotic processes in keratinocytes. However, the exact pathogenesis of alopecia areata requires further investigation. Recently, there has been an increasing focus on understanding the mechanisms of immune diseases resulting from the interplay between the nervous and the immune system. Neurogenic inflammation due to neuroimmune disorders of the skin system may disrupt the inflammatory microenvironment of the hair follicle, which plays a crucial part in the progression of alopecia areata.

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“…Kang et al, provide some initial insight into a potential role for toll‐like‐receptor signalling in AA . Herz‐Ruelas et al, examine the secretion of stress hormones in AA in response to ultra‐violet A (UVA‐1) phototherapy . These studies suggest that we need to look well beyond the lymphocyte infiltrate and investigate the role of the innate immune system, and the dynamics of hair follicle biology, to fully understand the mechanism(s) of AA pathogenesis as well as the responses to treatment.…”

Section: Alopecia Areatamentioning

confidence: 99%