Journal
CELL HOST & MICROBE
Volume 12, Issue 4, Pages 432-444Publisher
CELL PRESS
DOI: 10.1016/j.chom.2012.09.007
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Funding
- Yale Brown-Coxe and Anna Fuller postdoctoral fellowships
- National Institutes of Health grant [AI068041-06]
- Burroughs Wellcome Fund Investigator in the Pathogenesis of Infectious Disease Award [1007845]
- Searle Foundation Scholars Program [05-F-114]
- Cancer Research Institute Investigator Award Program [CRI06-10]
- Crohn's and Colitis Foundation of America Senior Investigator Award [R09928]
- W.W. Winchester Foundation
- MRC [MR/J006874/1] Funding Source: UKRI
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From plants to humans, the ability to control infection at the level of an individual cell-a process termed cell-autonomous immunity-equates firmly with survival of the species. Recent work has begun to unravel this programmed cell-intrinsic response and the central roles played by IFN-inducible GTPases in defending the mammalian cell's interior against a diverse group of invading pathogens. These immune GTPases regulate vesicular traffic and protein complex assembly to stimulate oxidative, autophagic, membranolytic, and inflammasome-related antimicrobial activities within the cytosol, as well as on pathogen-containing vacuoles. Moreover, human genome-wide association studies and disease-related transcriptional profiling have linked mutations in the Immunity-Related GTPase M (IRGM) locus and altered expression of guanylate binding proteins (GBPs) with tuberculosis susceptibility and Crohn's colitis.
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