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Treatment with an anti-CD44v10-specific antibody inhibits the onset of alopecia areata in C3H/HeJ mice
Author(s): Freyschmidt-Paul P, Seiter S, Zoller M, Konig A, Ziegler A, Sundberg JP, Happle R, Hoffmann R
Source: JOURNAL OF INVESTIGATIVE DERMATOLOGY    Volume: 115    Issue: 4    Pages: 653-657    Published: OCT 2000  
Times Cited: 23     References: 23     
Abstract: A murine CD44v10-neutralizing antibody has been reported to impair delayed-type hypersensitivity reactions. Because alopecia areata is characterized by a delayed-type hypersensitivity-like T cell mediated immune response, we addressed the question whether an anti-CD44v10-antibody influences the onset of alopecia areata. Therefore, we used the C3H/HeJ mouse model with the induction of alopecia areata in unaffected mice by the grafting of lesional alopecia areata mouse skin. Six grafted mice were injected (intraperitoneally) with anti-CD44v10, six grafted mice with anti-CD44standard, and six with phosphate-buffered saline only. After 11 wk phosphate-buffered saline injected animals on average had developed alopecia areata on 36.8% of their body. The onset of hair loss was slightly delayed and its extent reduced to 17.2% of their body in anti-CD44standard-treated mice. By contrast, five of six anti-CD44v10-treated mice did not show any hair loss and one mouse developed alopecia areata on only 1% of the body. Immunohistochemical examination revealed a marked reduction of perifollicular CD8(+) lymphocytes and, to a lesser degree, CD4(+) cells as well as a decreased expression of major histocompatibility complex class I on hair follicle epithelium in anti-CD44v10-treated mice as compared with phosphate-buffered saline or anti-CD44 standard-treated mice. Our data show that anti-CD44v10 is able to inhibit the onset of alopecia areata in C3H/HeJ mice. This might be accomplished by an anti-CD44v10-triggered impairment of immune cell homing (e.g., CD8(+) T cells), resulting in a decrease of their number in target tissues.
Document Type: Article
Language: English
Reprint Address: Freyschmidt-Paul, P (reprint author), Univ Marburg, Dept Dermatol, Deutschhausstr 9, D-35033 Marburg, Germany
Addresses:
1. Univ Marburg, Dept Dermatol, D-35033 Marburg, Germany
2. Univ Marburg, Inst Med Biometry & Epidemiol, D-35033 Marburg, Germany
3. Univ Homburg, Dept Dermatol, D-6650 Homburg, Germany
4. German Canc Res Ctr, Dept Tumor Progress & Immune Def, D-6900 Heidelberg, Germany
5. Jackson Lab, Bar Harbor, ME 04609 USA
Publisher: BLACKWELL SCIENCE INC, 350 MAIN ST, MALDEN, MA 02148 USA
Subject Category: Dermatology
IDS Number: 363CK
ISSN: 0022-202X
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