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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 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 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 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.

The skin protects the body, regulates temperature, senses touch, and makes vitamin D.

This case report describes a nine-year-old girl with juvenile dermatomyositis and alopecia areata, suggesting a possible etiological link between these coexisting immune-mediated diseases, a previously unreported association.

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 demonstrated that antigens from the skin bacterium Staphylococcus epidermidis can stimulate CD8+ T cells, which in turn enhance wound healing.

This study suggests that sweat glands may have an immune privilege similar to hair follicles, and disruptions in this could contribute to autoimmune skin diseases.

In this review, researchers conclude that immune imbalance between regulatory and cytotoxic T cells, along with activation of IFN-γ–MHC and IL-15–NK pathways, disrupts hair follicle immune privilege, suggesting pivotal mechanisms in alopecia areata development and potential targets for immunotherapeutic interventions.

This review discusses the mechanisms underlying the collapse of hair follicle immune privilege in alopecia areata and emphasizes the importance of therapeutic strategies aimed at restoring immune tolerance.

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

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, 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 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.

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.

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.

Hair loss treatment caused more hair loss in a man.

This study found that electrical epilation in organ-cultured human scalp skin perturbs hair follicles by causing inflammation, impairing melanin production, and possibly inhibiting post-epilation hair re-growth.

This study suggests that in alopecia areata, innate lymphoid cells type 1 may contribute to the disease’s pathogenesis by inducing hair follicle changes similarly to CD8+ T cells.

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.

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.

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.

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 alopecia areata is linked to genetic factors, specifically HLA haplotypes on chromosome 6, and involves immune privilege collapse at hair follicles which is mediated by the JAK-STAT pathway and pro-inflammatory cytokines like IFN-γ.

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.

This study found that activating hair follicle resident T cells in a human organ culture can induce an alopecia areata-like immune response, and that the drug farudodstat partially reduced this effect.

In this study, the researchers used a human hair follicle model to demonstrate that T cell stimulation can induce an alopecia areata–like phenotype, with cell proliferation and immune privilege collapse; however, the DHODH inhibitor farudodstat partially mitigated these effects by reducing T cell proliferation.

This study observed that dandruff-affected scalp skin has increased T-cell infiltration in the epidermis and a reduction in the hair follicle's physiological immune privilege, particularly in the suprabulbar outer root sheath area, indicating a distinct immune microenvironment compared to healthy scalp.