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This study found that diphencyprone showed a significant clinical response for treating alopecia areata, while tacrolimus was not effective.

In this study, the researchers identified a variant in the CCHCR1 gene associated with an alopecia areata subtype characterized by impaired keratinization and autoimmune events.

This study identified that mouse MILL1 and MILL2 are glycoproteins distinct from human MICA/B, primarily due to their association with β2-microglobulin and TAP-independent surface expression.

This study identified a specific genetic variant in the CCHCR1 gene that may contribute to alopecia areata through impaired keratinization, suggesting an alternative mechanism beyond autoimmune causes.

This paper proposes that the induction of HF-specific neo-antigens by peripheral CD8+ T cells may maintain self-tolerance but could also lead to immunopathology in conditions like alopecia areata.

This study found that RANKL signaling enhances CD8+ T cell-mediated anti-viral immunity during herpes simplex virus infection by preventing apoptosis of Langerhans cells, suggesting potential therapeutic applications.

This review outlines the advancements in organ and tissue transplantation since the discovery of the human MHC and reports no new clinical results.

This study suggests that the neuropeptide CGRP may protect against, but not restore, IFNγ-induced collapse of hair follicle immune privilege in alopecia areata.

This study suggests that SOCS3 treatment may effectively inhibit alopecia areata by suppressing CD8+ T cell activity and IFN-γ production.

This study reports that hair follicle-derived mesenchymal stem cells significantly reduced hair loss and inflammation in alopecia areata models, suggesting a potential therapeutic approach.

This case report describes a 29-year-old woman with longstanding alopecia areata who experienced improvement in her scalp hair loss after 7 years of topical treatment with squaric acid dibutylester.

This study found that targeting IL-6, IL-1, and CCR6 signaling pathways may effectively reduce irradiation-induced alopecia and dermatitis in radiotherapy patients.

In this study, hair follicle-derived mesenchymal stromal cells showed potential for immunomodulation, with equivalent or superior responses compared to those from adipose tissue, suggesting a promising alternative cell source.

This study reported that using UVB preirradiation and anti-CD154 antibody treatment in a humanized mouse model prolonged hair follicle allograft survival and reduced immune cell infiltration without needing generalized immunosuppression.

In this study, researchers observed that phospholipid-calcium carbonate hybrid nanoparticles effectively delivered Tofacitinib citrate topically, which significantly inhibited hair follicle apoptosis and promoted hair growth in a mouse model of chemotherapy-induced alopecia, compared to a traditional Tofacitinib solution.

Farudodstat may effectively treat alopecia areata without harmful side effects.

Farudodstat may effectively treat alopecia areata without harming hair follicles.

Farudodstat may help treat alopecia areata by protecting hair follicles.

This study observes that TYK2 inhibition with BMS-986202 may extend hair follicle growth phases and decrease inflammatory cell markers in alopecia areata, suggesting potential for clinical application.

This study found that interleukin-12 signals play a role in hair follicle immune privilege collapse in ex vivo alopecia areata models, and a TYK2 inhibitor may help prevent or reverse this process.

This study found that in an ex vivo model simulating alopecia areata, the DHODH inhibitor farudodstat reduced T-cell proliferation and MHC protein expression in hair follicles, suggesting it may protect against immune privilege collapse without cytotoxic effects.

Arg1+ macrophages may play a role in Alopecia Areata, offering new treatment targets.

This study suggests that human hair follicles may actively suppress natural killer cells, which contrasts with the observed defects in NK cell regulation in alopecia areata.

This study describes previously unknown immune characteristics of the normal human nail, highlighting its similarities to the hair follicle immune system and suggesting an immune privilege in the proximal nail matrix that both provides autoimmunity protection and presents infection susceptibility.

This study found that local injections of interleukin-4 and neutralizing anti-interferon-γ antibody effectively treated alopecia in a mouse model, suggesting potential therapeutic pathways for human alopecia areata.

This article argues that human scalp hair follicles could serve as a surrogate model for studying immune privilege in the human eye, offering a novel approach for ocular IP research.

This study found that immunity to self-prion peptides could be induced in Lewis rats, but in older rats, it was associated with severe skin inflammation and hair loss.

Sorafenib may cause hair loss in a way similar to alopecia areata.

This article discusses the immune privilege in hair follicles and suggests that restoring its collapse might be an effective strategy for treating alopecia areata and cicatricial alopecia, but it reports no new clinical results.