717 citations,
June 2010 in “Nature” A genome-wide association study conducted on 1,054 cases and 3,278 controls identified several susceptibility loci for alopecia areata, suggesting the involvement of both innate and adaptive immunity in the disease. The study highlighted significant associations with genes related to regulatory T cells, CTLA4, IL-2/IL-21, IL-2RA, and the HLA region, as well as genes expressed in the hair follicle like PRDX5 and STX17. Notably, the ULBP gene cluster on chromosome 6q25.1, encoding ligands for the natural killer cell receptor NKG2D, was implicated for the first time in autoimmune disease, with ULBP3 expression upregulated in the hair follicle during active disease. This research provided insights into the genetic basis of alopecia areata and suggested a novel mechanism involving ULBP ligand upregulation in autoimmunity.
69 citations,
May 2009 in “Journal of Investigative Dermatology” Stress might contribute to hair loss in alopecia areata.
253 citations,
December 2007 in “Journal of Investigative Dermatology” The study explored how hair follicles (HFs) maintain immune privilege (IP) to avoid natural killer (NK) cell attacks, which typically target cells with low MHC class I expression. It was found that HFs actively suppress NK cells, with the HF epithelium expressing the NK cell inhibitor macrophage migration inhibitory factor. In healthy individuals, fewer NK function-activating receptors and more inhibitory receptors were present compared to those with alopecia areata (AA), an autoimmune disease linked to a breakdown of HF-IP. AA patients showed increased NK cell activity around hair follicles, suggesting a defect in NK cell inhibition that contributes to the disease's pathogenesis. This defect was previously unreported and highlighted the need for considering NK cell activity in AA management.
159 citations,
December 2007 in “American Journal of Pathology” Stress-related substance P may lead to hair loss and negatively affect hair growth.
286 citations,
August 2007 in “Journal of Clinical Investigation” The study of alopecia areata provided insights into autoimmunity, particularly regarding immune privilege and the interaction between genetics and neuroimmunology. Alopecia areata was identified as a T cell–mediated autoimmune disease affecting hair follicles, with disease onset linked to the collapse of hair follicle immune privilege in humans and animal models. The research reviewed the involvement of HLA associations, other immunogenetic factors, and neuroendocrine parameters in the disease's pathogenesis, highlighting its significance as a model disease for the immunology community.
76 citations,
March 2005 in “Journal of Molecular Medicine” Certain mice without specific receptors or mast cells don't lose hair from stress.
64 citations,
July 1997 in “Journal of The American Academy of Dermatology” Finding eosinophils near hair bulbs helps diagnose alopecia areata.