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There is additional evidence that distinct CD44 isoforms interfere with the extravasation of selective leukocyte subsets. We wanted to explore this question in alopecia areata (AA), a hair-follicle centric autoimmune disease, and in a chronic eczema. The question became of interest because AA is treated efficiently by topical application of a contact sensitizer, such that a mild DTH reaction is maintained persistently. Aiming to support the therapeutic efficacy of a chronic eczema in AA by anti-CD44 treatment, it became essential to control whether a blockade of migration, preferentially of AA effector cells, could be achieved by CD44 isoform-specific antibodies. Anti-panCD44 and anti-CD44 variant 10 isoform (CD44v10) inhibited in vitro migration of leukocytes from untreated and allergen-treated, control and AA mice. In vivo, both antibodies interfered with T cell and monocyte extravasation into the skin; only anti-panCD44 prevented T cell homing into lymph nodes. Contributing factors are disease-dependent alterations in chemokine\/chemokine receptor expression and a blockade of CD44 on endothelial cells and leukocytes. It is important that CD44 can associate with several integrins and ICAM-1. Associations depend on CD44 activation and vary with CD44 isoforms and leukocyte subpopulations. CD44 standard isoform preferentially associates with CD49d in T cells and CD44v10 with CD11b in monocytes. Accordingly, anti-panCD44 and anti-CD49d inhibit T cell, anti-CD11b, and anti-CD44v10 macrophage migration most efficiently. Thus, allergen treatment of AA likely can be supported by targeting AA T cells selectively via a panCD44-CD49d-bispecific antibody.<\/jats:p>","DOI":"10.1189\/jlb.0107063","type":"journal-article","created":{"date-parts":[[2007,4,19]],"date-time":"2007-04-19T01:04:03Z","timestamp":1176944643000},"page":"57-71","source":"Crossref","is-referenced-by-count":29,"title":["Anti-CD44-mediated blockade of leukocyte migration in skin-associated immune diseases"],"prefix":"10.1093","volume":"82","author":[{"given":"Margot","family":"Z\u00f6ller","sequence":"first","affiliation":[{"name":"Department of Tumor Progression and Tumor Defense, German Cancer Research Center , Heidelberg , Germany"},{"name":"Department of Applied Genetics, University of Karlsruhe , Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pooja","family":"Gupta","sequence":"additional","affiliation":[{"name":"Department of Tumor Progression and Tumor Defense, German Cancer Research Center , Heidelberg , Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rachid","family":"Marhaba","sequence":"additional","affiliation":[{"name":"Department of Tumor Progression and Tumor Defense, German Cancer Research Center , Heidelberg , Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mario","family":"Vitacolonna","sequence":"additional","affiliation":[{"name":"Department of Tumor Progression and Tumor Defense, German Cancer Research Center , Heidelberg , Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Pia","family":"Freyschmidt-Paul","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University Hospital Marburg , Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2007,4,18]]},"reference":[{"key":"2023033006514880400_","doi-asserted-by":"crossref","first-page":"371","DOI":"10.1111\/j.1600-0625.1999.tb00385.x","article-title":"Alopecia areata: an autoimmune disease?","volume":"8","author":"McElwee","year":"1999","journal-title":"Exp. 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