期刊
IMMUNITY
卷 23, 期 3, 页码 249-262出版社
CELL PRESS
DOI: 10.1016/j.immuni.2005.08.001
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资金
- NHLBI NIH HHS [P01 HL 59561, T32 HL 66987] Funding Source: Medline
- NIAID NIH HHS [R21 AI 54933, AI 45587, U54 AI 57159] Funding Source: Medline
Perforin delivers granzymes to induce target-cell apoptosis. At high concentrations, perforin multimerizes in the plasma membrane to form pores. However, whether granzymes enter target cells via membrane pores is uncertain. Here we find that perforin at physiologically relevant concentrations and during cell-mediated lysis creates pores in the target-cell membrane, transiently allowing Ca2+ and small dyes into the cell. The Ca2+ flux triggers a wounded membrane-repair response in which internal vesicles, including lysosomes and endosomes, donate their membranes to reseal the damaged membrane. Perforin also triggers the rapid endocytosis of granzymes into large EEA-1-staining vesicles. The restoration of target-cell membrane integrity by triggering the repair response is necessary for target cells subjected to cytotoxic T lymphocyte attack to avoid necrosis and undergo the slower process of programmed cell death. Thus, the target cell actively participates in determining its own fate during cell-mediated death.
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