| 1. |
- Hagnerud, Sven, et al.
(författare)
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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 migration.
- 2006
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Ingår i: Journal of Immunology. - 0022-1767. ; 176:10, s. 5772-8
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Tidskriftsartikel (refereegranskat)abstract
- 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 alpha, 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(high)CD11b(high)CD8alpha(-)CD4(+) DCs. These DCs correspond to marginal zone DCs and express signal regulatory protein alpha, 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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| 2. |
- Olsson, Mattias, et al.
(författare)
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Hematologic Diseases : Autoimmune Hemolytic Anemia and Immune Thrombocytopenic Purpura
- 2006
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Ingår i: Immunogenetics of Autoimmune Disease. - 0387360042
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Bokkapitel (övrigt vetenskapligt/konstnärligt)abstract
- SummaryAutoinimune destruction of circularing blood cells in autoummunc hemolytic anemia (AIHA) and immune thrombocytopenic purpura (ITP) is often seen in autoirnnsune diseases and lymhoid malignancies. Erythrocytes or platelets that arc recognized by autoantibodues are rapidly phagocytosed by rnacrophages. Although much is known about the mechanisms behind macrophage-mediated destruction of sensitized blood cells, 1ess is known about the genetics behind AIHA and ITP. We here review what is known about the ethiology of Al 1-IA and lip, with particular emphasis on the role olgenetic factors behind auroanribody production. 1 cell activation and apoptosis, and Fcy receptor polymorphisms. The importance of inhibitory regulation oi rnacrophagcs through CD47IS[RPa interaction, and its significance for autoirnmune hemarological disease is also discussed.
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