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Deficit of CD47 Results in a Defect of Marginal Zone Dendritic Cells, Blunted Immune Response to Particulate Antigen and Impairment of Skin Dendritic Cell Migration¹

Sven Hagnerud^2,*, Partha Pratim Manna^2,, Marina Cella, Åsa Stenberg^*, William A. Frazier, Marco Colonna and Per-Arne Oldenborg^3,*

^* Department of Integrative Medical Biology, Section for Histology and Cell Biology, Umeå University, Umeå, Sweden; and Department of Biochemistry and Molecular Biophysics and Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110

CD47 is a ubiquitously expressed cell surface glycoprotein that associates with integrins and regulates chemotaxis, migration, and activation of leukocytes. CD47 is also a ligand for signal regulatory protein , a cell surface receptor expressed on monocytes, macrophages, granulocytes, and dendritic cell (DC) subsets that regulates cell activation, adhesion, and migration. Although the function of CD47 in macrophages and granulocytes has been studied in detail, little is known about the role of CD47 in DC biology in vivo. In this study we demonstrate that CD47^–/– mice exhibit a selective reduction of splenic CD11c^highCD11b^highCD8^–CD4⁺ DCs. These DCs correspond to marginal zone DCs and express signal regulatory protein , possibly explaining their selective deficiency in CD47^–/– mice. Deficiency of marginal zone DCs resulted in impairment of IgG responses to corpusculate T cell-independent Ags. Although epidermal DCs were present in normal numbers in CD47^–/– mice, their migration to draining lymph nodes in response to contact sensitization was impaired, while their maturation was intact. In vitro, CD47^–/– mature DCs showed normal CCR7 expression but impaired migration to CCL-19, whereas immature DC response to CCL-5 was only slightly impaired. These results demonstrate a fundamental role of CD47 in DC migration in vivo and in vitro and in the function of marginal zone DCs.

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