151 citations
,
February 2007 in “International Journal of Dermatology” This review explores the causes and mechanisms of alopecia areata and discusses current treatments, reporting no new clinical findings.
143 citations
,
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.
375 citations
,
July 2006 in “Journal of Investigative Dermatology” This review discusses the brain-skin connection, the skin's role in stress response, and highlights unmet challenges in understanding stress-induced skin inflammation but reports no new experimental findings.
24 citations
,
May 2006 in “Journal of Investigative Dermatology” This study found that allergen treatment in alopecia areata mice appeared to alter leukocyte subset distribution and impaired dendritic cell migration, which may affect T-cell activation and hair follicle recovery.
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.
127 citations
,
December 2005 in “Experimental Dermatology” This study provides evidence that psychoemotional stress inhibits hair growth in mice by affecting the brain-hair follicle axis, with specific neuropeptides and treatments modulating this effect.
293 citations
,
November 2005 in “Trends in Immunology” This study indicates that stress in mice recruits specific neuroimmunoendocrine elements, leading to neurogenic skin inflammation that inhibits hair growth and highlights the skin's role in stress response research.
139 citations
,
October 2005 in “Journal of Investigative Dermatology” 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.
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.
76 citations
,
March 2005 in “Journal of Molecular Medicine” This study found that premature hair loss due to stress does not occur in NK-1 receptor knockout or mast cell deficient mice, suggesting a key role for neurokinin substance P and mast cell interaction in stress-related hair follicle changes.
108 citations
,
July 2004 in “American Journal of Pathology” This study suggests that nerve growth factor plays a crucial role in the stress-induced termination of hair growth in mice, and its antagonism might offer a therapeutic approach to mitigate stress-related hair loss.
29 citations
,
January 2004 in “Experimental Dermatology” In this study, anthralin treatment led to hair regrowth in alopecia areata-like affected C3H/HeJ mice, suggesting it may be an effective therapy for this condition.
12 citations
,
November 2003 in “Journal of the American Academy of Dermatology” This study found hair regrowth in the majority of AA-affected mice and rats treated with diphencyprone, suggesting its potential utility for understanding human alopecia areata and the drug's therapeutic action.
148 citations
,
September 2003 in “Journal of Investigative Dermatology Symposium Proceedings” Alopecia areata is an autoimmune disorder causing hair loss, linked to specific hair follicle antigens and genetic factors.
86 citations
,
December 2002 in “Tissue Antigens” In this study, researchers found that the AIRE G961C variant is a significant risk factor for severe alopecia areata and early-onset cases, particularly in patients with alopecia universalis.
275 citations
,
November 2002 in “International Journal of Dermatology” This study found that among an Asian population with alopecia areata, commonly first episodes occurred before age 40, with severe cases linked to psychological effects and treatments showing significant regrowth.
114 citations
,
August 2002 in “Journal of Investigative Dermatology” Alopecia areata is caused by an immune response, and targeting immune cells might help treat it.
77 citations
,
June 2002 in “Journal of Investigative Dermatology” CD44 variant changes start alopecia areata, but don't maintain it.
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.
131 citations
,
November 1998 in “The journal of investigative dermatology/Journal of investigative dermatology” This study observed that alopecia areata can be induced and serially transferred in C3H/HeJ mice using skin grafts, providing a useful model for studying the disease in humans.
89 citations
,
October 1996 in “Dermatologic Clinics” This review discusses androgenetic alopecia and alopecia areata through a systems biology lens, emphasizing the role of multi-omics data integration to explore molecular mechanisms and potential therapeutic strategies, but offers no new clinical results.
122 citations
,
April 1995 in “Journal of Cutaneous Pathology” The document describes how to tell different types of non-scarring hair loss apart by looking at hair and scalp tissue under a microscope.
60 citations
,
February 1992 in “British Journal of Dermatology” In this study, serum from patients with alopecia areata or universalis did not affect hair growth in transplanted scalp skin grafts on nude mice, despite increased deposition of immunoreactants.
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.