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Prepublished online as a Blood First Edition Paper on September 26, 2002; DOI 10.1182/blood-2002-05-1586. This Article Full Text (PDF) All Versions of this Article: 2002-05-1586v1 101/3/801    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Christopherson, K. W Articles by Hromas, R. A Search for Related Content PubMed PubMed Citation Articles by Christopherson, K. W Articles by Hromas, R. A Social Bookmarking                   What's this? Submitted May 29, 2002 Accepted September 3, 2002 Endothelial induction of the T-cell chemokine CCL21 in T-cell autoimmune diseases Kent W Christopherson, Antoinette F Hood, Jeffrey B Travers, Heather Ramsey, and Robert A Hromas* Department of Microbiology & Immunology and the Walther Oncology Center, Indiana University Medical Center, Indianapolis, IN, USA Department of Dermatology and the Wells Center for Pediatric Research, Indiana University Medical Center, Indianapolis, IN, USA Division of Hematology/Oncology and Walther Oncology Center, Indiana University Medical Center, Indianapolis, IN, USA * Corresponding author; email: rhromas{at}iupui.edu. The signals which mediate T-cell infiltration during T-cell auto-immune diseases are poorly understood. The chemokine CCL21 (originally isolated by us and others as Exodus-2/6Ckine/SLC/TCA4) is highly potent and highly specific for attracting T-cell migration. However, it is thought to be expressed only in secondary lymphoid organs, directing naive T-cells to areas of antigen presentation. It is not thought to play a role in T-cell effector function during a normal immune response. In this study we tested the expression of T-cell chemokines and their receptors during T-cell auto-immune infiltrative skin diseases. Using immunohistology it was found that the expression of CCL21 but not CCL19 or 20 was highly induced in endothelial cells of T-cell auto-immune diseases. The receptor for CCL21, CCR7, was also found to be highly expressed on the infiltrating T-cells, the majority of which expressed the memory CD45Ro phenotype. These data imply that the usual loss of CCL21 responsiveness in the normal development of memory T-cell effector function does not hold for auto-immune skin diseases. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. K. Damas, C. Smith, E. 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