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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 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 Citation Map 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., II Articles by Hromas, R. A. Related Collections Cell Adhesion and Motility Chemokines, Cytokines, and Interleukins Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 February 2003, Vol. 101, No. 3, pp. 801-806 CHEMOKINES Endothelial induction of the T-cell chemokine CCL21 in T-cell autoimmune diseases Kent W. Christopherson II, Antoinette F. Hood, Jeffrey B. Travers, Heather Ramsey, and Robert A. Hromas From the Department of Microbiology and Immunology and the Walther Oncology Center, Department of Dermatology and the Wells Center for Pediatric Research, Division of Hematology/Oncology and Walther Oncology Center, Indiana University Medical Center, Indianapolis. The signals that mediate T-cell infiltration during T-cell autoimmune 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 stimulating 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 autoimmune infiltrative skin diseases. By using immunohistology it was found that the expression of CCL21 but not CCL19 or 20 was highly induced in endothelial cells of T-cell autoimmune diseases. The receptor for CCL21, CCR7, was also found to be highly expressed on the infiltrating T cells, most 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 autoimmune skin diseases. © 2003 by The American Society of Hematology.   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. Oie, B. Fevang, B. Halvorsen, T. Waehre, A. Boullier, U. Breland, A. Yndestad, O. Ovchinnikova, et al. Enhanced Expression of the Homeostatic Chemokines CCL19 and CCL21 in Clinical and Experimental Atherosclerosis: Possible Pathogenic Role in Plaque Destabilization Arterioscler. Thromb. Vasc. Biol., March 1, 2007; 27(3): 614 - 620. [Abstract] [Full Text] [PDF] T. Raine, P. Zaccone, P. Mastroeni, and A. Cooke Salmonella typhimurium Infection in Nonobese Diabetic Mice Generates Immunomodulatory Dendritic Cells Able to Prevent Type 1 Diabetes J. Immunol., August 15, 2006; 177(4): 2224 - 2233. 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