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Blood, 15 September 2007, Vol. 110, No. 6, pp. 2005-2012. Prepublished online as a Blood First Edition Paper on June 8, 2007; DOI 10.1182/blood-2006-12-062448. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-12-062448v1 110/6/2005    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 Blanchet, M.-R. Articles by McNagny, K. M. Search for Related Content PubMed PubMed Citation Articles by Blanchet, M.-R. Articles by McNagny, K. M. Related Collections Immunobiology Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY CD34 facilitates the development of allergic asthma Marie-Renée Blanchet1, Steven Maltby1, D. James Haddon1, Helen Merkens1, Lori Zbytnuik1, and Kelly M. McNagny1 1 The Biomedical Research Centre, University of British Columbia, Vancouver, Canada Asthma is a pulmonary inflammatory disease dependent on eosinophil and mast cell infiltration into the lung. CD34 is a sialomucin expressed by both of these cell types, and we have used CD34–/– mice and a standard mouse model of asthma to evaluate the importance of CD34 expression on disease development. In comparison with wild-type (wt) mice, CD34–/– mice exhibited a dramatic reduction in all hallmarks of allergic asthma, including lowered airway inflammatory cell infiltration, airway hyperresponsiveness, and mast-cell recruitment. Bone marrow transplantation experiments confirmed that these defects are due to CD34 expression by bone marrow–derived cells. This was not, however, due to an inability to respond to antigen as, on a per cell basis, wt and CD34–/– inflammatory cells exhibit identical responses in cytokine production. We found a striking reduction in mobility of CD34–/– eosinophils in vitro, the major component of inflammatory infiltrates, which was consistent with proposed models for CD34 as an inhibitor of cell-cell adhesion. In summary, our data suggest that CD34 enhances mast-cell and eosinophil invasiveness and that its expression by these cells is a prerequisite for development of allergic asthma. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. J. Haddon, F. Antignano, M. R. Hughes, M.-R. Blanchet, L. Zbytnuik, G. Krystal, and K. M. McNagny SHIP1 Is a Repressor of Mast Cell Hyperplasia, Cytokine Production, and Allergic Inflammation In Vivo J. Immunol., July 1, 2009; 183(1): 228 - 236. [Abstract] [Full Text] [PDF] J. L. Bennett, M.-R. Blanchet, L. Zhao, L. Zbytnuik, F. Antignano, M. Gold, P. Kubes, and K. M. McNagny Bone Marrow-Derived Mast Cells Accumulate in the Central Nervous System During Inflammation but Are Dispensable for Experimental Autoimmune Encephalomyelitis Pathogenesis J. Immunol., May 1, 2009; 182(9): 5507 - 5514. [Abstract] [Full Text] [PDF] J. S. Nielsen and K. M. McNagny Novel functions of the CD34 family J. Cell Sci., November 15, 2008; 121(22): 3683 - 3692. [Abstract] [Full Text] [PDF] S. C. Kerr, C. B. Fieger, K. R. Snapp, and S. D. Rosen Endoglycan, a Member of the CD34 Family of Sialomucins, Is a Ligand for the Vascular Selectins J. Immunol., July 15, 2008; 181(2): 1480 - 1490. [Abstract] [Full Text] [PDF] E. Gounaris, S. E. Erdman, C. Restaino, M. F. Gurish, D. S. Friend, F. Gounari, D. M. Lee, G. Zhang, J. N. Glickman, K. Shin, et al. Mast cells are an essential hematopoietic component for polyp development PNAS, December 11, 2007; 104(50): 19977 - 19982. [Abstract] [Full Text] [PDF]

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