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...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1996-11, Vol.274 (5288), p.795-798
Main Authors: Lindberg, Frederik P., Bullard, Daniel C., Caver, Tony E., Gresham, Hattie D., Beaudet, Arthur L., Brown, Eric J.
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Analysis of the immune response. Humoral and cellular immunity
Animals
Antigens, CD - genetics
Antigens, CD - immunology
Antigens, CD - physiology
Bacteria
Biological and medical sciences
Carrier Proteins - genetics
Carrier Proteins - immunology
CD47 Antigen
Cell Movement
Erythrocytes
Escherichia coli
Escherichia coli Infections - immunology
Female
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Gene Targeting
Genetics
Genotypes
Heterozygote
Heterozygotes
Human migration
Immunity, Innate
Immunobiology
Infections
Integrin beta3
Integrins
Ligands
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Migration
Molecular Sequence Data
Natural immunity
Neutrophil Activation
Neutrophils
Neutrophils - immunology
Neutrophils - physiology
Organs and cells involved in the immune response
Peptide Fragments - pharmacology
Peritonitis - immunology
Phagocytosis
Phenotype
Physiological aspects
Platelet Membrane Glycoproteins - physiology
Proteins
Respiratory Burst
Rodents
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Summary: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 $\beta_3$ 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.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.274.5288.795