CD47 is upregulated on circulating hematopoietic stem cells and leukemia cells to avoid phagocytosis

Macrophages clear pathogens and damaged or aged cells from the blood stream via phagocytosis. Cell-surface CD47 interacts with its receptor on macrophages, SIRPalpha, to inhibit phagocytosis of normal, healthy cells. We find that mobilizing cytokines and inflammatory stimuli cause CD47 to be transie...

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Podrobná bibliografia
Vydané v:Cell Ročník 138; číslo 2; s. 271
Hlavní autori: Jaiswal, Siddhartha, Jamieson, Catriona H M, Pang, Wendy W, Park, Christopher Y, Chao, Mark P, Majeti, Ravindra, Traver, David, van Rooijen, Nico, Weissman, Irving L
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 23.07.2009
Predmet:
Animals
Antibodies, Monoclonal
CD47 Antigen - immunology
Cell Survival
fms-Like Tyrosine Kinase 3
Hematopoietic Stem Cells - immunology
Humans
Macrophages - immunology
Mice
Neoplasm Transplantation
Neoplastic Stem Cells - immunology
Phagocytosis
Protein-Tyrosine Kinases - chemistry
Receptors, Immunologic
Transplantation, Heterologous
Up-Regulation
ISSN:1097-4172, 1097-4172
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Popis
Shrnutí:Macrophages clear pathogens and damaged or aged cells from the blood stream via phagocytosis. Cell-surface CD47 interacts with its receptor on macrophages, SIRPalpha, to inhibit phagocytosis of normal, healthy cells. We find that mobilizing cytokines and inflammatory stimuli cause CD47 to be transiently upregulated on mouse hematopoietic stem cells (HSCs) and progenitors just prior to and during their migratory phase, and that the level of CD47 on these cells determines the probability that they are engulfed in vivo. CD47 is also constitutively upregulated on mouse and human myeloid leukemias, and overexpression of CD47 on a myeloid leukemia line increases its pathogenicity by allowing it to evade phagocytosis. We conclude that CD47 upregulation is an important mechanism that provides protection to normal HSCs during inflammation-mediated mobilization, and that leukemic progenitors co-opt this ability in order to evade macrophage killing.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1097-4172
1097-4172
DOI:10.1016/j.cell.2009.05.046