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Infection and Immunity, March 2007, p. 1144-1153, Vol. 75, No. 3
0019-9567/07/$08.00+0     doi:10.1128/IAI.00869-06

Improved Antibacterial Host Defense and Altered Peripheral Granulocyte Homeostasis in Mice Lacking the Adhesion Class G Protein Receptor CD97

Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute,¹ Laboratory of Host Defenses,² Laboratory of Immunoregulation, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20878³

Received 31 May 2006/ Returned for modification 17 July 2006/ Accepted 29 November 2006

CD97 is a member of the adhesion family of G protein-coupled receptors. Alternatively spliced forms of CD97 bind integrins 5ß1 and vß3, decay accelerating factor, or dermatan sulfate. CD97 is expressed on myeloid cells at high levels and a variety of other cell types at lower levels. Little is known about the physiological function of CD97. To begin dissecting the function of CD97, we evaluated the immune response of CD97 null mice to systemic infection by Listeria monocytogenes. CD97 null mice were significantly more resistant to listeriosis than matched wild-type mice. A major determinant of the difference in survival appeared to be the comparatively more robust accumulation of granulocytes in the blood and in infected livers of CD97 null mice within 18 h of inoculation, correlating with a decrease in the number of bacteria. CD97 null mice also displayed a mild granulocytosis in the nonchallenged state. Because there is a strong suggestion that CD97 functions in an adhesive capacity, we examined the migratory properties of granulocytes in CD97 null mice. In chimeric animals, CD97 null and wild-type granulocytes migrated similarly, as determined by inflammation-induced emigration from the bone marrow and accumulation in the peritoneum. Granulocyte development in the bone marrow of CD97 null mice was comparable to that of wild-type mice, and CD97 deficiency did not appear to stimulate granulocytosis secondary to peripheral inflammation and resultant granulocyte colony-stimulating factor induction, unlike various other models of adhesion deficiencies. Our results suggest that CD97 plays a role in peripheral granulocyte homeostasis.

Published ahead of print on 11 December 2006.

Editor: R. P. Morrison