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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.

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

Linalool in personal care products may worsen frontal fibrosing alopecia by damaging hair follicle stem cells and triggering harmful immune responses.

Ritlecitinib reduces alopecia areata symptoms by blocking JAK3/TEC signaling and T-cell activity.

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.

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.

Farudodstat may help treat alopecia areata by protecting hair follicles.

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

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.

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.

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 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.

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

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.

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 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.

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

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.

Linalool in fragrances may harm hair follicles and contribute to hair loss.

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.

This research developed new in vitro models for high-throughput screening of drugs that could protect or restore immune privilege in hair follicles, finding that Tofacitinib was effective in preventing inflammation-related marker upregulation, while Tacrolimus and αMSH worked specifically in outer root sheath keratinocytes.

In ex vivo organ culture of human scalp hair follicles, this study found that IL-9 signaling inhibits hair growth, reduces progenitor cell generation, and disrupts immune privilege.

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 reports that stress-related neurohormones and factors, such as CRH and SP, can inhibit hair growth and alter immune functions in murine and human hair follicles.

This study found that treatment with EGFR inhibitors or mitogen-activated kinase inhibitors may compromise the immune privilege of human scalp hair follicles, suggesting new directions for managing drug-induced folliculitis.