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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 study provided 18 evidence-based recommendations for managing acne vulgaris, strongly endorsing treatments like benzoyl peroxide, topical retinoids, and oral isotretinoin for severe cases, and issued conditional recommendations for therapies like salicylic acid and spironolactone, while offering good practice statements on combining treatment methods.

Hair loss treatment caused more hair loss in a man.

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

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

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 observed an increasing trend of young patients with androgenetic alopecia visiting dermatologists, with genetic factors and abnormal androgen metabolism in the scalp contributing to its development.

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 reported an increase in female androgenic alopecia patients in their forties and found stress-related factors, particularly work tasks, associated with AGA in both male and female patients.

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 review highlights advances in understanding alopecia areata as a systemic disease involving genetic, immune, and environmental factors, noting new treatments like Janus kinase inhibitors but acknowledging challenges in long-term safety and accessibility.

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.

In this study, pair housing of rhesus macaques after intrafacility transfer reduced some undesirable behaviors and diarrhea compared to single housing, although no cortisol level differences were observed.

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.

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

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

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

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 describes a new hair transplant technique combining FUT and FUE to increase graft numbers in patients with high levels of baldness and reduced scalp laxity, but it does not report clinical outcomes.

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 review discusses recent genome-wide association studies identifying novel candidate genes for various forms of alopecia, providing insights into their pathogenesis and molecular mechanisms, but reports no new clinical results.

This article introduces the concept of follicular units, highlighting their significance in hair restoration, but reports no new findings.