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Blood, 15 March 2004, Vol. 103, No. 6, pp. 2214-2220.
Prepublished online as a Blood First Edition Paper on November 26, 2003; DOI 10.1182/blood-2003-08-2978.
Submitted September 3, 2003
Accepted November 5, 2003
Mast cell-mediated inflammatory responses require the  2 1 integrin
Brian T Edelson, Zhengzhi Li, Loretta K Pappan, and Mary M Zutter*
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, USA
Department of Cell Biology, Washington University School of Medicine, St. Louis, MO, USA
Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN, USA; Department of Cancer Biology, Vanderbilt University School of Medicine, Nashville, TN, USA
* Corresponding author; email: mary.zutter{at}vanderbilt.edu.
Although the  2 1 integrin is widely expressed and has been extensively studied, it has not been previously implicated in mast cell biology. We observed that 2 integrin subunit-deficient mice exhibited markedly diminished neutrophil and IL-6 responses during Listeria monocytogenes- and zymosan-induced peritonitis. Since exudative neutrophils of wild-type mice expressed little 21 integrin, it seemed unlikely that this integrin mediated neutrophil migration directly. Here we demonstrate constitutive 21 integrin expression on peritoneal mast cells. Although 2-null mice contain normal numbers of peritoneal mast cells, these 2-null cells do not support in vivo mast cell-dependent inflammatory responses. We conclude that 21 integrin provides a costimulatory function required for mast cell activation and cytokine production in response to infection.
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