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Blood, 1 April 2008, Vol. 111, No. 7, pp. 3562-3570. Prepublished online as a Blood First Edition Paper on January 15, 2008; DOI 10.1182/blood-2007-08-107664. This Article Full Text (PDF) All Versions of this Article: blood-2007-08-107664v1 111/7/3562    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 McCall-Culbreath, K. D. Articles by Zutter, M. M. Search for Related Content PubMed PubMed Citation Articles by McCall-Culbreath, K. D. Articles by Zutter, M. M. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted August 16, 2007 Accepted January 3, 2008 Cross-talk between the 21 integrin and c-met/HGF-R regulates innate immunity Karissa D. McCall-Culbreath, Zhengzhi Li, and Mary M. Zutter* Departments of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN, United States Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN, United States Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, United States * Corresponding author; email: mary.zutter{at}vanderbilt.edu. Data from a number of investigators suggest that the 21 integrin, a receptor for collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-1 (MMP-1), endorepellin and several viruses, is required for innate immunity and regulation of autoimmune/allergic disorders. We demonstrated that the innate immune response to Listeria monocytogenes required 21 integrin expression by peritoneal mast cells (PMCs). Ligation of the 21 integrin by C1q contained in immune complexes comprised of Listeria and antibody was required for PMC activation in vitro and in vivo. However, ligation of the 21 integrin alone was insufficient to activate cytokine secretion, suggesting that one or more additional signals emanating from a co-receptor were required for PMC activation. Here, we demonstrate that C1q, but neither other complement proteins nor FcR, is required for early innate immune response to Listeria. The binding of Listeria's Internalin B (InlB) to hepatocyte growth factor receptor (HGF-R)/c-met provides the costimulatory function required for PMC activation. Either HGF or Listeria InlB bound to c-met and either C1q or type I collagen bound to 21 integrin stimulate PMC activation. These findings suggest that cross-talk between c-met and the 21 integrin may contribute to mast cell activation in autoimmune and inflammatory disorders. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Nystrom, Z. P. Shaik, D. Gullberg, T. Krieg, B. Eckes, R. Zent, A. Pozzi, and R. V. Iozzo Role of tyrosine phosphatase SHP-1 in the mechanism of endorepellin angiostatic activity Blood, November 26, 2009; 114(23): 4897 - 4906. [Abstract] [Full Text] [PDF] J. D. San Antonio, J. J. Zoeller, K. Habursky, K. Turner, W. Pimtong, M. Burrows, S. Choi, S. Basra, J. S. Bennett, W. F. DeGrado, et al. A Key Role for the Integrin {alpha}2{beta}1 in Experimental and Developmental Angiogenesis Am. J. Pathol., September 1, 2009; 175(3): 1338 - 1347. [Abstract] [Full Text] [PDF]

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