Toll-like receptors in control of immunological autophagy

被引:129
作者
Delgado, M. A. [1 ]
Deretic, V. [1 ]
机构
[1] Univ New Mexico, Dept Mol Genet & Microbiol, Hlth Sci Ctr, Albuquerque, NM 87131 USA
基金
美国国家卫生研究院;
关键词
autophagy; TLR; immunity; inflammation; BCL-X-L; ADAPTIVE IMMUNITY; MYCOBACTERIUM-TUBERCULOSIS; INNATE IMMUNITY; CROHNS-DISEASE; CELL-DEATH; GENE ATG5; BECLIN; MACROPHAGES; RECOGNITION;
D O I
10.1038/cdd.2009.40
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Autophagy is a cell biological process, enabling cells to autodigest their own cytosol when starved, remove cytoplasmic protein aggregates too large for proteasomal degradation, eliminate aberrant or over-proliferated organelles, and sanitize the cytoplasm by killing intracellular microbes. The role of autophagy has been expanded in recent years to include diverse immunological effector and regulatory functions. In this review, we summarize the multiple immunological roles of autophagy uncovered to date and focus primarily on details of induction of autophagy by pattern recognition receptors, as a newly established Toll-like receptor output. Taken together with other links between autophagy and innate and adaptive immunity processes, this cell-autonomous antimicrobial defense may be evolutionarily positioned at the root of immunity with the multiple innate and adaptive immunity connections uncovered to date reflecting a co-evolution of this ancient cell-defense mechanism and more advanced immunological systems in metazoans. Cell Death and Differentiation (2009) 16, 976-983; doi: 10.1038/cdd.2009.40; published online 15 May 2009
引用
收藏
页码:976 / 983
页数:8
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