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The Journal of Immunology, 1998, 161: 6463-6467.
Copyright © 1998 by The American Association of Immunologists


CUTTING EDGE

Cutting Edge: Impaired Mast Cell Development and Innate Immunity in Mac-1 (CD11b/CD18, CR3)-Deficient Mice1

Alexander R. Rosenkranz*, Angela Coxon2,*, Marcus Maurer2,{ddagger}, Michael F. Gurish{dagger}, K. Frank Austen{dagger}, Daniel S. Friend{ddagger}, Stephen J. Galli{ddagger} and Tanya N. Mayadas3,*

Departments of * Pathology and {dagger} Medicine, Brigham and Women’s Hospital, and {ddagger} Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115

Mac-1 (CD11b/CD18, CR3), a ß2 integrin expressed on leukocytes, is important in leukocyte migration. We demonstrate that Mac-1 is also expressed on peritoneal mast cells and LPS stimulated bone marrow-derived cultured mast cells, and that Mac-1-deficient mice, which lack this receptor, have significant reductions in the numbers of mast cells resident in the peritoneal cavity, peritoneal wall, and dorsal skin. The reduced numbers of mast cells in Mac-1-deficient mice may have important functional consequences, in that Mac-1-deficient mice exhibit significantly increased mortality after cecal ligation and puncture, a model of acute septic peritonitis in which host resistance has been shown to be dependent on both mast cells and complement. These findings demonstrate that Mac-1 is required for the expression of normal levels of mast cells in the peritoneal cavity, peritoneal wall, and certain areas of the skin, as well as for maintaining adequate mast cell-dependent host defense against bacterial infection.




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