Alopecia areata

Freyschmidt‐Paul, Pia; McElwee, Kevin J.; Hoffmann, Rolf

doi:10.1007/3-211-27377-8_19

Cited by 3 publications

(4 citation statements)

References 181 publications

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Section: Mechanisms Of Hf Ipmentioning

confidence: 99%

“…HFs may also have the ability to block lymphocyte activity through the Fas‐Fas ligand (FasL) system, as identified in eye graft models 134‐136 . In fact, mice with mutations in Fas or FasL are largely resistant to the development of AA: When skin from mice with non‐functional Fas or FasL are grafted to AA‐affected mice, the grafted skin remains resistant to AA and hair continues to grow from the grafted skin 136 . Also of note, inhibition of Fas/FasL‐mediated apoptotic signalling by the main component of Astragalus membranaceus, a medicinal plant with anti‐inflammatory, anti‐oxidant, anti‐viral, and anti‐apoptotic properties, improved hair growth in a mouse model of non‐inflammatory hair loss 137 .…”

Section: Mechanisms Of Hf Ipmentioning

confidence: 99%

“…For example, the immunosuppressive drug FK506 (tacrolimus) 334,335 downregulates MHC class I expression and has been shown to protect HFs from IFNγ‐induced IP collapse in ex vivo studies 76 . Despite some success in rodent models, 336,337 clinical trials with topical FK506 have been unsuccessful, probably due to poor skin penetration 338‐340 . However, in a case report systemic FK506 produced a hair growth response 341 .…”

Section: Therapeutic Perspectivesmentioning

confidence: 99%

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Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

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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: Mechanisms Of Hf Ipmentioning

confidence: 99%

Section: Mechanisms Of Hf Ipmentioning

confidence: 99%

Section: Therapeutic Perspectivesmentioning

confidence: 99%

See 1 more Smart Citation

Hair follicle immune privilege and its collapse in alopecia areata

Bertolini

McElwee

Gilhar

et al. 2020

Experimental Dermatology

Self Cite

182

157

View full text Add to dashboard Cite

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“…Im Erwachsenenalter kann bei perakutem Verlauf (Pull−Test positiv, Verlauf seit 1 ± 3 Monaten) zunächst eine topische Thera− pie mit Kortikosteroiden der Wirkklasse III und IV (z. B. Mometason, Amcinonid; Clobetasol− 17−Propionat) je nach Akuität und Befall über 4 ± 6 Wochen angewandt werden (Evidenzlevel III[22]). In einer relativ neuen Studie zur Anwen− Die Therapie ist jedoch relativ schmerzhaft, verlangt häufige Visitentermine und ist im Bereich frontal der Transversallinie kontraindiziert (Emboliege− fahr der A. retinalis od.…”

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