Human IRGM induces autophagy to eliminate intracellular mycobacteria

被引:715
作者
Singh, Sudha B.
Davis, Alexander S.
Taylor, Gregory A.
Deretic, Vojo [1 ]
机构
[1] Univ New Mexico, Sch Med, Dept Mol Genet & Microbiol, Albuquerque, NM 87131 USA
[2] Univ New Mexico, Sch Med, Dept Cell Biol & Physiol, Albuquerque, NM 87131 USA
[3] Duke Univ, Dept Med, Durham, NC 27710 USA
[4] Duke Univ, Dept Microbiol & Mol Genet, Durham, NC 27710 USA
[5] Duke Univ, Dept Immunol, Durham, NC 27710 USA
[6] Duke Univ, Ctr Study Aging, Durham, NC 27710 USA
[7] Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Durham, NC 27710 USA
关键词
D O I
10.1126/science.1129577
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Immunity-related p47 guanosine triphosphatases (IRG) play a role in defense against intracellular pathogens. We found that the murine Irgm1 (LRG-47) guanosine triphosphatase induced autophagy and generated large autolysosomal organelles as a mechanism for the elimination of intracellular Mycobacterium tuberculosis. We also identified a function for a human IRG protein in the control of intracellular pathogens and report that the human Irgm1 ortholog, IRGM, plays a role in autophagy and in the reduction of intracellular bacillary load.
引用
收藏
页码:1438 / 1441
页数:4
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