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 Blood, 1 January 2006, Vol. 107, No. 1, pp. 143-150.
Prepublished online as a Blood First Edition Paper on September 15, 2005; DOI 10.1182/blood-2005-06-2218.

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IMMUNOBIOLOGY

Novel collectin/C1q receptor mediates mast cell activation and innate immunity

Brian T. Edelson, Thomas P. Stricker, Zhengzhi Li, S. Kent Dickeson, Virginia L. Shepherd, Samuel A. Santoro, and Mary M. Zutter

From the Departments of Pathology and Immunology, Washington University School of Medicine, St Louis, MO; and the Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN.

Mast cells play a critical role in innate immunity, allergy, and autoimmune diseases. The receptor/ligand interactions that mediate mast cell activation are poorly defined. The {alpha}2{beta}1 integrin, a receptor for collagens, laminins, decorin, E-cadherin, matrix metalloproteinase-1 (MMP-1), endorepellin, and several viruses, has been implicated in normal developmental, inflammatory, and oncogenic processes. We recently reported that {alpha}2 integrin subunit–deficient mice exhibited markedly diminished neutrophil and IL-6 responses during Listeria monocytogenes–and zymosan-induced peritonitis. Peritoneal mast cells require {alpha}2{beta}1 integrin expression for activation in response to pathogens, yet the ligand and molecular mechanisms by which the {alpha}2{beta}1 integrin induces activation and cytokine secretion remain unknown. We now report that the {alpha}2{beta}1 integrin is a novel receptor for multiple collectins and the C1q complement protein. We demonstrate that the {alpha}2{beta}1 integrin provides a costimulatory function required for mast cell activation and cytokine secretion. This finding suggests that the {alpha}2{beta}1 integrin is not only important for innate immunity but may serve as a critical target for the regulation of autoimmune/allergic disorders.


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Mast cells: must they always be different?
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Blood 2006 107: 1-2. [Full Text] [PDF]



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