143 citations
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January 2007 in “The American Journal of Human Genetics” This study identified four genetic loci on chromosomes 6, 10, 16, and 18 that may contribute to susceptibility for alopecia areata and suggested shared genetic factors with psoriasis.
44 citations
,
December 2005 in “Journal of Investigative Dermatology” 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.
20 citations
,
November 2005 in “Journal of Investigative Dermatology Symposium Proceedings” This study found that IFN-γ plays a critical role in T cell activation and the pathogenesis of alopecia areata in C3H/HeJ mice.
185 citations
,
August 2005 in “Autoimmunity Reviews” This review discusses alopecia areata as a model for studying tissue-directed autoimmune diseases and reports no new clinical findings.
23 citations
,
March 2001 in “Clinics in dermatology” This study found that 363 genes were differentially expressed in alopecia areata skin compared to non-lesional skin, suggesting T-cell mediated immune responses and distinct gene profiles related to the disease's stage.
127 citations
,
January 2000 in “Journal of Investigative Dermatology” This study found that pro-inflammatory cytokines and apoptotic mechanisms, specifically involving granzyme B and Fas pathways, are associated with chronic alopecia areata, indicating their potential role in the disease's persistence.
5 citations
,
January 1994 in “Dermatology” This study found that severe forms of alopecia areata showed increased activated T cells and natural killer cells, which decreased after corticosteroid treatment, correlating with disease activity and hair regrowth.
68 citations
,
December 1983 in “British Journal of Dermatology” This study found HLA and beta 2-microglobulin antigens in various skin structures, with specific localization patterns in keratinocytes and hair follicle components, but not in eccrine or apocrine glands.