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

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 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.

Different substances affect hair and skin cell growth in various ways, with some promoting and others inhibiting cell proliferation.

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 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 found that immune privilege collapse in the hair follicle bulge and associated immune responses may contribute significantly to the pathogenesis of lichen planopilaris, suggesting a potential autoimmune basis for the disease.

In this study, researchers found that quiescent stem cells resist immune attack due to downregulated antigen presentation, which may help explain the immune evasion of early cancer-initiating cells.

In this study, researchers found that substance P triggered premature catagen development and immune changes in human scalp hair follicles, providing a possible biological link between stress and hair loss conditions like telogen effluvium and alopecia areata.

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 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 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 found significant associations between certain MICA variants and haplotypes with alopecia areata, suggesting MICA as a potential candidate gene linked to the disease's susceptibility and severity.

This study reports that in primary cicatricial alopecias, increased expression of certain immune markers in the hair-follicle bulge suggests a collapse of immune privilege, which may contribute to follicle destruction.

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 analysis reports that hepatitis B surface protein antigen exposure is associated with an increased risk of alopecia areata.

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

This review discusses oxidative stress in alopecia areata pathogenesis and potential treatment strategies, reporting no new clinical results but suggesting biomarkers for oxidative stress and discussing JAK inhibitors as promising options.

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.

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 suggests that genetic overlap between alopecia areata and major depressive disorder may be limited to the MHC region, highlighting the need for further research.

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, the CYP 21A2 gene p.V281L mutation was associated with an increased susceptibility to familial frontal fibrosing alopecia, suggesting an antigen-driven mechanism linked to certain human leukocyte antigen haplotypes.

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 reports that two mouse models of scarring alopecia exhibit similar patterns of hair loss progression despite histological differences in inflammatory cell localization and MHC class I expression.