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Lymphocytes, neuropeptides, and genes involved in alopecia areata
Amos Gilhar, … , Ralf Paus, Richard S. Kalish
Amos Gilhar, … , Ralf Paus, Richard S. Kalish
Published August 1, 2007
Citation Information: J Clin Invest. 2007;117(8):2019-2027. https://doi.org/10.1172/JCI31942.
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Science in Medicine Article has an altmetric score of 9

Lymphocytes, neuropeptides, and genes involved in alopecia areata

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Abstract

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.

Authors

Amos Gilhar, Ralf Paus, Richard S. Kalish

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Figure 2

A model of immune privilege collapse in AA pathogenesis.

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A model of immune privilege collapse in AA pathogenesis.
Both a normal a...
Both a normal anagen (growing) hair follicle (A) and a hair follicle in AA (B) are shown. MHC class I molecules are expressed on the epidermis, and on the most superficial (distal) portion of the normal hair follicle epithelium. The inferior (proximal) portions of the hair follicle are immune privileged and deficient in expression of MHC classes I and II as well as APCs. By contrast, the AA anagen hair follicle expresses MHC class I and II molecules throughout the follicular epithelium, including the portion adjacent to the dermal papilla of the hair follicle. Active AA also exhibits a perifollicular infiltrate of CD4+ T cells and an intrafollicular infiltrate of CD8+ T cells. IRS, inner root sheath; ORS, outer root sheath.

Copyright © 2025 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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Referenced in 4 patents
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