Decreased resistance to bacterial infection and granulocyte defects in IAP-deficient mice.
Granulocyte [polymorphonuclear leucocyte (PMN)] migration to sites of infection and subsequent activation is essential for host defense. Gene-targeted mice deficient for integrin-associated protein (IAP, also termed CD47) succumbed to Escherichia coli peritonitis at inoccula survived by heterozygous littermates. In vivo, they had an early defect in PMN accumulation at the site of infection. In vitro, IAP-/- PMNs were deficient in beta3 integrin-dependent ligand binding, activation of an oxidative burst, and Fc receptor-mediated phagocytosis. Thus, IAP plays a key role in host defense by participating both in PMN migration in response to bacterial infection and in PMN activation at extravascular sites.
Lindberg
F P
FP
Department of Infectious Diseases, Washington University School of Medicine, St. Louis, MO 63110, USA.
Bullard
D C
DC
Caver
T E
TE
Gresham
H D
HD
Beaudet
A L
AL
Brown
E J
EJ
D000595:Amino Acid Sequence; D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000276:immunology* / Q000502:physiology; D051928:CD47 Antigen; D002352:Carrier Proteins / Q000235:genetics / Q000276:immunology*; D002465:Cell Movement; D004927:Escherichia coli Infections / Q000276:immunology*; D005260:Female; D018390:Gene Targeting; D006579:Heterozygote; D007113:Immunity, Innate; D039661:Integrin beta3; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D018375:Neutrophil Activation; D009504:Neutrophils / Q000276:immunology* / Q000502:physiology; D010446:Peptide Fragments / Q000494:pharmacology; D010538:Peritonitis / Q000276:immunology; D010587:Phagocytosis; D010641:Phenotype; D010980:Platelet Membrane Glycoproteins / Q000502:physiology; D016897:Respiratory Burst
D015703:Antigens, CD; D051928:CD47 Antigen; D002352:Carrier Proteins; C497895:Cd47 protein, mouse; D039661:Integrin beta3; D010446:Peptide Fragments; D010980:Platelet Membrane Glycoproteins