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Table of Contents
Vol. 66, No. 2, 1998
Issue release date: March – April
Section title: Original Paper
Pathobiology 1998;66:90–107
(DOI:10.1159/000028002)

Comparison of Alopecia areata in Human and Nonhuman Mammalian Species

McElwee K.J.a · Boggess D.a · Olivry T.b · Oliver R.F.f · Whiting D.c · Tobin D.J.g · Bystryn J.-C.d · King Jr. L.E.e · Sundberg J.P.a
a The Jackson Laboratory, Bar Harbor, Me., b Department of Companion Animal and Special Species Medicine, North Carolina State University College of Veterinary Medicine, Raleigh, N.C., c Dallas Associated Dermatologists, Dallas, Tex., d Department of Dermatology, New York University, New York, N.Y., and e Department of Dermatology, Vanderbilt University, Nashville, Tenn., USA; f Department of Biological Sciences, University of Dundee, and g Department of Biomedical Sciences, University of Bradford, UK

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: May 20, 1998
Issue release date: March – April

Number of Print Pages: 18
Number of Figures: 9
Number of Tables: 4

ISSN: 1015-2008 (Print)
eISSN: 1423-0291 (Online)

For additional information: http://www.karger.com/PAT

Abstract

Alopecia areata (AA) is a nonscarring form of inflammatory hair loss in humans. AA-like hair loss has also been observed in other species. In recent years the Dundee experimental bald rat and the C3H/HeJ mouse have been put forward as models for human AA. AA in all species presents with a wide range of clinical features from focal, locally extensive, diffuse hair loss, to near universal alopecia. Histologically, all species have dystrophic anagen stage hair follicles associated with a peri- and intrafollicular inflammatory cell infiltrate. Autoantibodies directed against anagen stage hair follicle structures are a consistent finding. Observations on AA pathogenesis suggest nonhuman species can provide excellent models for the human disease. Ultimately, animal models will be used to determine the genetic basis of AA, potential endogenous and/or environmental trigger(s), mechanism(s) of disease initiation and progression, and allow rapid evaluation of new and improved disease treatments.


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: May 20, 1998
Issue release date: March – April

Number of Print Pages: 18
Number of Figures: 9
Number of Tables: 4

ISSN: 1015-2008 (Print)
eISSN: 1423-0291 (Online)

For additional information: http://www.karger.com/PAT


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