Hair growth in scalp grafts from patients with alopecia areata and alopecia universalis grafted onto nude mice

Gilhar, Amos

doi:10.1001/archderm.123.1.44

Cited by 41 publications

(27 citation statements)

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“…Grafting of hairless scalp from AA patients to nude mice results in dramatic regrowth of human hair (49). This was explained by the removal of immunologic influence from the hair follicles but does not distinguish whether a humoral or cellular immune pathogenesis underlies AA.…”

Section: Hair Follicle Autoantibodiesmentioning

confidence: 99%

Lymphocytes, neuropeptides, and genes involved in alopecia areata

Gilhar¹,

Paus²,

Kalish³

2007

J. Clin. Invest.

268

278

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Many lessons in autoimmunity -particularly relating to the role of immune privilege and the interplay between genetics and neuroimmunology -can be learned from the study of alopecia areata, the most common cause of inflammation-induced hair loss. Alopecia areata is now understood to represent an organ-restricted, T cell-mediated autoimmune disease of hair follicles. Disease induction is associated with collapse of hair follicle immune privilege in both humans and in animal models. Here, the role of HLA associations, other immunogenetic factors, and neuroendocrine parameters in alopecia areata pathogenesis are reviewed. This instructive and clinically significant model disease deserves more widespread interest in the immunology community.Nonstandard abbreviations used: AA, alopecia areata; AIRE, autoimmune regulator; APECED, autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy; IP-10, IFN-g-inducible protein 10; MIC, MHC class I chain-related; MIF, macrophage migration inhibitory factor; α-MSH, α-melanocyte-stimulating hormone; NALP1, NACHT leucine-rich-repeat protein 1; NGF, nerve growth factor.

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Section: Hair Follicle Autoantibodiesmentioning

confidence: 99%

Lymphocytes, neuropeptides, and genes involved in alopecia areata

Gilhar¹,

Paus²,

Kalish³

2007

J. Clin. Invest.

268

278

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show abstract

“…21 Hair loss after grafting occurs with grafts of human scalp to humans (transplants) or mice. In the published experience of Gilhar and Krueger 22 with grafts of human scalp to immunodeficient mice, the number of hairs regrowing from a 2-mm graft is insufficient for analysis, whereas there is adequate hair regrowth from grafts of involved alopecia scalp. For this reason, it was not possible to perform these experiments with noninvolved, or normal, scalp explants.…”

Section: Commentmentioning

confidence: 99%

Mediation of Alopecia Areata by Cooperation Between CD4+ and CD8+ T Lymphocytes

Gilhar¹,

Landau²,

Assy³

et al. 2002

Arch Dermatol

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“…3 Although the exact etiology of AA is still unknown, there is accumulated evidence that supports a hereditary susceptibility and an autoimmune pathogenesis, such as a familial history in 4-27%, 4,5 and the increased frequency of other autoimmune diseases, particularly autoimmune thyroid disease, and of organspecific autoantibodies in patients with AA [6][7][8] as well as the presence of CD8 + T cells next to the hair follicles. 9,10 Among the various immunomodulatory treatments that have been used to induce remission in AA, systemic corticosteroids have been administered in extensive or rapidly progressive AA and in alopecia totalis/universalis. 11,12 Systemic oral corticosteroids have been reported to be effective in extensive AA, but relapses occurred when the dosage was reduced.…”

Section: Introductionmentioning

confidence: 99%