Journal
SCIENCE
Volume 332, Issue 6030, Pages 717-721Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1201711
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Funding
- NIH National Institute of Allergy and Infectious Diseases [R01 AI068041-01A1]
- Burroughs Wellcome Fund
- Searle Scholars Program
- Cancer Research Institute
- W.W. Winchester Foundation
- Browne-Cox Fellowship
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Immune interferon gamma (IFN-gamma) is essential for mammalian host defense against intracellular pathogens. IFN-gamma induces nearly 2000 host genes, yet few have any assigned function. Here, we examined a complete mouse 65-kilodalton (kD) guanylate-binding protein (Gbp) gene family as part of a 43-member IFN-gamma-inducible guanosine triphosphatase (GTPase) superfamily in mouse and human genomes. Family-wide loss-of-function analysis found that at least four Gbps-Gbp1, Gbp6, Gbp7, and Gbp10-conferred cell-autonomous immunity to listerial or mycobacterial infection within macrophages and gene-deficient animals. These Gbps solicited host defense proteins, including the phagocyte oxidase, antimicrobial peptides, and autophagy effectors, to kill intracellular bacteria. Thus, specific 65-kD Gbps coordinate a potent oxidative and vesicular trafficking program to protect the host from infection.
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