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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 3

Proposed pathogenesis of AA.

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Proposed pathogenesis of AA.
Cytokines and cellular factors responsible ...
Cytokines and cellular factors responsible for maintaining immune privilege are listed in the left box. Those factors believed to mediate loss of immune privilege and initiation of disease are listed in the middle box. Loss of immune privilege is associated with expression of MHC class I molecules, which are capable of presenting hair follicle autoantigens to T lymphocytes. Secondary autoimmune amplification circuits that may help establish or amplify the pathology are listed in the right box.

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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