Autophagy in immune cell regulation and dysregulation

被引:15
作者
Chaturvedi, Akanksha [1 ]
Pierce, Susan K. [1 ]
机构
[1] NIAID, Immunogenet Lab, NIH, Rockville, MD 20852 USA
关键词
TOLL-LIKE RECEPTORS; DENDRITIC CELLS; SELF-DIGESTION; GENE ATG5; T-CELLS; STARVATION; DISEASE; ANTIGEN; MICE; RECOGNITION;
D O I
10.1007/s11882-009-0050-1
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Autophagy is an ancient pathway required for cell and tissue homeostasis and differentiation. Initially thought to be a process leading to cell death, autophagy is currently viewed as a beneficial catabolic process that promotes cell survival under starvation conditions by sequestering components of the cytoplasm, including misfolded proteins, protein aggregates, and damaged organelles, and targeting them for lysosome-mediated degradation. In this way, autophagy plays a role in maintaining a balance between degradation and recycling of cellular material. The importance of autophagy is underscored by the fact that malfunctioning of this pathway results in neurodegeneration, cancer, susceptibility to microbial infection, and premature aging. Autophagy occurs in almost all cell types, including immune cells. Recent advances in the field suggest that autophagy plays a central role in regulating the immune system at multiple levels. In this review, we focus on recent developments in the area of autophagy-mediated modulation of immune responses.
引用
收藏
页码:341 / 346
页数:6
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