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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, 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.

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

Farudodstat may effectively treat alopecia areata without harmful side effects.

Farudodstat may effectively treat alopecia areata without harming 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.

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

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

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 found that immune privilege is preserved in hair follicles of nonsegmental vitiligo patients compared to those with alopecia areata, potentially protecting follicular melanocytes from autoimmune attacks.

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 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 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 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 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.

This research suggests that innate lymphoid cells type 1 (ILC1) may contribute to the development of alopecia areata, alongside CD8+ T cells, by disrupting hair follicle immune privilege and promoting features of the disease.

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.

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 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.

This study observed that dandruff is linked to a weakened immunoprivilege in hair follicles, with reduced Langerhans cells and increased epidermal CD4+ and CD8+ T cell infiltration.

This study found that the proprietary aptamer TAGX-0003 significantly inhibited IFNγ-induced effects in pre-clinical human models of alopecia areata, promoting hair regrowth and potentially preventing disease relapse.

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 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 indicates that CD4 protein may have a functional role in basal cell-like keratinocytes through TCR/CD3-independent signaling, affecting their proliferation, differentiation, and migration.

This study found that a TYK2 inhibitor, BMS-986202, may restore immune privilege in hair follicles and promote hair regrowth in a humanized alopecia areata mouse model by inhibiting IL-12-mediated signaling.

This article reviews the roles of lesser-known secreted phospholipase A2 isoforms in various biological processes, such as immune suppression, metabolic regulation, epidermal hyperplasia, and male reproduction, without reporting new clinical findings.