期刊
NATURE IMMUNOLOGY
卷 10, 期 5, 页码 461-470出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.1726
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资金
- US National Institutes of Health [R01 CA074730, R01 CA096511, R01 AI054483, R01 AI065982, U54 AI057160, R01 AI151267, R01 CA109618]
- Howard Hughes Medical Institute
- Ellison Medical Foundation
- NATIONAL CANCER INSTITUTE [R01CA096511, R01CA074730, R01CA109618] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI051367, R01AI065982, R01AI054483, U54AI057160] Funding Source: NIH RePORTER
In its classical form, autophagy is a pathway by which cytoplasmic constituents, including intracellular pathogens, are sequestered in a double-membrane-bound autophagosome and delivered to the lysosome for degradation. This pathway has been linked to diverse aspects of innate and adaptive immunity, including pathogen resistance, production of type I interferon, antigen presentation, tolerance and lymphocyte development, as well as the negative regulation of cytokine signaling and inflammation. Most of these links have emerged from studies in which genes encoding molecules involved in autophagy are inactivated in immune effector cells. However, it is not yet known whether all of the critical functions of such genes in immunity represent 'classical autophagy' or possible as-yet-undefined autophagolysosome-independent functions of these genes. This review summarizes phenotypes that result from the inactivation of autophagy genes in the immune system and discusses the pleiotropic functions of autophagy genes in immunity.
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