Mica

This study identified an association between alopecia areata and the MICA*009 and HLA-B14 genetic markers, highlighting the importance of studying them together to better understand their role in this condition.

This study reports a strong association between the MICA locus, specifically the MICA∗3-DR∗6-DQ6 haplotype, and Alopecia Areata in families.

This study suggests that allergens like linalool found in personal care products may contribute to the pathobiology of frontal fibrosing alopecia by affecting immune responses and stem cell function in hair follicles.

This pilot study suggests that lovastatin may counteract stress-induced MICA expression in hair follicles and enhance MICA shedding, potentially offering a complementary approach for alopecia areata treatment.

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

This study reviewed recent theories on alopecia areata's pathogenesis, highlighting its autoimmune nature due to immune privilege disruption in hair follicles, and noted current treatments have limited efficacy with high relapse rates, underscoring the need for further research into its mechanisms for better therapies.

This review explores animal models of alopecia areata, particularly focusing on the insights they've provided into the disease's immune mechanisms and potential treatment approaches, without reporting new experimental data.

Apremilast may help treat hair loss in alopecia areata.

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.

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 case report suggests that anidulafungin may be associated with hair loss, highlighting the need for physicians to monitor this potential adverse effect.

This study suggests that human dermal Vδ1+ γδ T-cells may contribute to alopecia areata pathogenesis by targeting stressed scalp hair follicles and inducing immune privilege collapse.

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 study suggests that linalool, a common allergen in personal care products, may contribute to frontal fibrosing alopecia pathogenesis by triggering immune responses and depleting hair follicle stem cells, especially in sensitized individuals.

This review outlines the proposed theories behind the development of alopecia areata, emphasizing the autoimmune process involving lost immune privilege in hair follicles, and stresses the need to pinpoint specific pathogenic mechanisms for potential treatments.

This study suggests a connection between the unfolded protein response and upregulation of NKG2D ligands in stressed hair follicles, highlighting a potential role of PRDX5 in alopecia areata pathogenesis.

This case report describes a 6-year-old boy with a scalp infection caused by Candida parapsilosis, which was successfully treated with 2% ketoconazole ointment after other treatments failed; antifungal susceptibility testing showed variable drug resistance.

This case report is the first to associate HAIR-AN syndrome with polycystic ovaries, Hashimoto’s thyroiditis, and several metabolic conditions in a 21-year-old woman, emphasizing early diagnosis and management.

This conference proceeding abstract provides no new research results, focusing only on event details from the British Association of Dermatology's Forty-Sixth Annual Meeting held in Oxford in 1966.