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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 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 review discusses the role of immune privilege collapse in the pathogenesis of alopecia areata, emphasizing the potential for therapeutic manipulation of hair bulb immune privilege to offer new treatment options, and reports no new results.

This article reviews the role of vasoactive intestinal peptide in maintaining immune privilege in hair follicles and does not report new findings; the authors propose it as essential for immune homeostasis in alopecia areata.

This study identified somatostatin as a potential secretory factor contributing to the immune privilege of human hair follicles.

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 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 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 found that human hair follicle cells suppress immune activity, with somatostatin playing a significant role, suggesting potential applications for treating inflammatory hair loss conditions.

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 review discusses immune privilege in anagen hair follicles and its collapse in alopecia areata, emphasizing the importance of restoring this function for effective management and disease relapse prevention.

This study suggests that cultured hair follicle dermal sheath cup cells exhibit immune privilege properties, partly through the expression of PD-L1, which impacts co-cultured immune cells' behavior.

This review examines the literature on autoimmune hair loss disorders, highlighting the collapse of immune privilege and the potential role of neurogenic stress in this process, but reports no new clinical results.

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 developed a technique to limit genetic recombination to regulatory T cells to investigate whether self-tolerance is maintained in non-lymphoid tissues, an area previously not well understood.

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 article compares the immunology of cancer and the placenta and suggests that immunotherapy for pregnant cancer patients could be feasible with careful exploration, though no new clinical results are reported.

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 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.

This study tested a hydrogel microneedle patch delivering T reg attractants in mice with alopecia, finding it boosted regulatory T cell numbers at the site, leading to hair regrowth without causing peripheral immunosuppression, suggesting a potential new approach for autoimmune skin disease treatment.

This study found that inhibiting EGFR and MEK in hair follicles may lead to a partial collapse of the immune privilege in the follicles and increased secretion of IL-33.

Farudodstat may effectively treat alopecia areata without harming hair follicles.

Farudodstat may help treat alopecia areata by protecting hair follicles.

This study suggests that NKG2D+ Vδ1 T cells may contribute to hair follicle pathology in alopecia areata by recognizing stressed keratinocytes and inducing immune privilege collapse.

This study provides a framework for understanding different types of alopecias based on immune privilege collapse at specific follicular sites, revealing distinct patterns in immune effector programs and stromal influences depending on the alopecia type.

This study found that human γδTregs promoted hair regrowth and restored hair follicle immune privilege in a model of alopecia areata, suggesting potential for cell-based therapy in autoimmune diseases.

In this review, summarized findings suggest that emerging targeted immunotherapies may offer promising treatment options for alopecia areata by addressing the breakdown of hair follicle immune privilege.

Ritlecitinib may help treat alopecia areata by protecting hair follicles.

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.