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This article was retracted on March 1, 2008. Blood, 1 January 2007, Vol. 109, No. 1, pp. 22-30. Prepublished online as a Blood First Edition Paper on September 12, 2006; DOI 10.1182/blood-2006-04-015206. This Article Full Text Full Text (PDF) Retraction (v111,p2537) All Versions of this Article: blood-2006-04-015206v1 109/1/22    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 Matsuyama, W. Articles by Arimura, K. Search for Related Content PubMed PubMed Citation Articles by Matsuyama, W. Articles by Arimura, K. Related Collections Immunobiology Phagocytes Cell Adhesion and Motility Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CLINICAL TRIALS AND OBSERVATIONS Discoidin domain receptor 1 contributes to eosinophil survival in an NF-B–dependent manner in Churg-Strauss syndrome Wataru Matsuyama1,, Hideo Mitsuyama1, Mikiko Ono1, Yuko Shirahama1, Ikkou Higashimoto1, Mituhiro Osame1, and Kimiyoshi Arimura1 1 Division of Respiratory Medicine, Respiratory and Stress Care Center, Kagoshima University Hospital, Japan Churg-Strauss syndrome (CSS) is a systemic disease that shows marked eosinophilia along with eosinophil infiltration in the tissue. Prolonged eosinophil survival plays an important role in the pathogenesis of CSS; however, its detailed molecular mechanism remains unclear. Discoidin domain receptor 1 (DDR1) is a receptor tyrosine kinase, and its ligand is collagen. DDR1 was expressed in human leukocytes and fibroblasts, and it plays an important role in leukocyte cytokine production and fibroblast survival in an NF-B–dependent manner. In this study, we examined in vitro and in vivo eosinophil DDR1 expression and its function in CSS patients. The expression level of DDR1 was significantly higher in the eosinophils of CSS patients, and the predominant isoform was DDR1b. Immunohistochemical findings revealed that the tissue-infiltrating eosinophils expressed endogenous DDR1. In CSS patients, DDR1 activation inhibited Fas agonistic antibody–induced apoptosis and up-regulated Fas agonistic antibody–induced cytokine production of eosinophils in an NF-B–dependent manner. Suppression of DDR1 expression in the eosinophils by using RNA interference and addition of the DDR1-blocking protein abolished these effects. We propose that DDR1 contributes to the eosinophil survival in the tissue microenvironment of CSS and that it might be involved in the development of CSS. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. A. Gomez-Puerta and X. Bosch Anti-Neutrophil Cytoplasmic Antibody Pathogenesis in Small-Vessel Vasculitis: An Update Am. J. Pathol., November 1, 2009; 175(5): 1790 - 1798. [Abstract] [Full Text] [PDF]

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