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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.

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IMMUNOBIOLOGY

Crosstalk between the {alpha}2β1 integrin and c-met/HGF-R regulates innate immunity

Karissa D. McCall-Culbreath1, Zhengzhi Li2, and Mary M. Zutter1,3

Departments of1 Microbiology and Immunology 2 Pathology, and 3 Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN

Data from several investigators suggest that the {alpha}2β1 integrin, a receptor for collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-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 {alpha}2β1 integrin expression by peritoneal mast cells (PMCs). Ligation of the {alpha}2β1 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 {alpha}2β1 integrin alone was insufficient to activate cytokine secretion, suggesting that one or more additional signals emanating from a coreceptor were required for PMC activation. Here, we demonstrate that C1q, but neither other complement proteins nor FcR{gamma}, 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 {alpha}2β1 integrin stimulates PMC activation. These findings suggest that crosstalk between c-met and the {alpha}2β1 integrin may contribute to mast-cell activation in autoimmune and inflammatory disorders.


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