Autophagy, Immunity, and Microbial Adaptations

被引:1009
作者
Deretic, Vojo [1 ]
Levine, Beth [2 ,3 ,4 ]
机构
[1] Univ New Mexico, Dept Mol Genet & Microbiol, Hlth Sci Ctr, Albuquerque, NM 87131 USA
[2] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA
[3] Univ Texas SW Med Ctr Dallas, Dept Microbiol, Dallas, TX 75390 USA
[4] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA
基金
美国国家卫生研究院;
关键词
HEPATITIS-C VIRUS; CELL-DEATH; BECLIN; FRANCISELLA-TULARENSIS; CHLAMYDIA-TRACHOMATIS; CROHNS-DISEASE; PHOSPHATIDYLINOSITOL; 3-PHOSPHATE; REGULATES AUTOPHAGY; TOXOPLASMA-GONDII; HOST-DEFENSE;
D O I
10.1016/j.chom.2009.05.016
中图分类号
Q93 [微生物学];
学科分类号
071005 [微生物学];
摘要
Autophagy adjusts cellular biomass and function in response to diverse stimuli, including infection. Autophagy plays specific roles in shaping immune system development, fueling host innate and adaptive immune responses, and directly controlling intracellular microbes as a cell-autonomous innate defense. As an evolutionary counterpoint, intracellular pathogens have evolved to block autophagic microbicidal defense and subvert host autophagic responses for their survival or growth. The ability of eukaryotic pathogens to deploy their own autophagic machinery may also contribute to microbial pathogenesis. Thus, a complex interplay between autophagy and microbial adaptations against autophagy governs the net outcome of host-microbe encounters.
引用
收藏
页码:527 / 549
页数:23
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