Journal
CURRENT OPINION IN IMMUNOLOGY
Volume 22, Issue 3, Pages 321-325Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.coi.2010.03.005
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Funding
- National Institutes of Health [AI50506, AI63419]
- Arthritis National Research Foundation
- National Multiple Sclerosis Society
- NATIONAL CANCER INSTITUTE [P30CA062203, T32CA009054] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI050606, R01AI063419, R01AI050506] Funding Source: NIH RePORTER
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Autophagy, an ancient cellular response where autophagic vacuoles are formed within the cytosol, is induced in response to a variety of cellular insults, including growth factor or nutrient withdrawal, organelle damage, and misfolded proteins. Autophagy is rapidly induced in T lymphocytes following antigenic stimulation and blockade of autophagic signaling greatly reduces T cell clonal expansion, suggesting that autophagy is primarily involved in promoting T cell survival. In contrast, a recently identified negative feedback loop involving FADD and caspase-8 limits the level of autophagy in T cells. Failure to activate caspase-8 during T cell mitogenesis leads to hyperactive autophagy and cellular death through a programmed necrotic mechanism. These findings suggest that crosstalk between these cellular processes is essential for T cell activation and homeostasis.
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