Treatment with an anti-CD44v10-specific antibody inhibits the onset of alopecia areata in C3H/HeJ mice

Citation
P. Freyschmidt-paul et al., Treatment with an anti-CD44v10-specific antibody inhibits the onset of alopecia areata in C3H/HeJ mice, J INVES DER, 115(4), 2000, pp. 653-657
Citations number
23
Categorie Soggetti
Dermatology,"da verificare
Journal title
JOURNAL OF INVESTIGATIVE DERMATOLOGY
ISSN journal
0022202X → ACNP
Volume
115
Issue
4
Year of publication
2000
Pages
653 - 657
Database
ISI
SICI code
0022-202X(200010)115:4<653:TWAAAI>2.0.ZU;2-E
Abstract
A murine CD44v10-neutralizing antibody has been reported to impair delayed- type hypersensitivity reactions. Because alopecia areata is characterized b y a delayed-type hypersensitivity-like T cell mediated immune response, we addressed the question whether an anti-CD44v10-antibody influences the onse t of alopecia areata. Therefore, we used the C3H/HeJ mouse model with the i nduction of alopecia areata in unaffected mice by the grafting of lesional alopecia areata mouse skin. Six grafted mice were injected (intraperitoneal ly) with anti-CD44v10, six grafted mice with anti-CD44standard, and six wit h phosphate-buffered saline only. After 11 wk phosphate-buffered saline inj ected animals on average had developed alopecia areata on 36.8% of their bo dy. The onset of hair loss was slightly delayed and its extent reduced to 1 7.2% 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 deve loped alopecia areata on only 1% of the body. Immunohistochemical examinati on revealed a marked reduction of perifollicular CD8(+) lymphocytes and, to a lesser degree, CD4(+) cells as well as a decreased expression of major h istocompatibility complex class I on hair follicle epithelium in anti-CD44v 10-treated mice as compared with phosphate-buffered saline or anti-CD44 sta ndard-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 cel ls), resulting in a decrease of their number in target tissues.