CTL: Caspases terminate life, but that's not the whole story

Tissue Antigens

Volumn 59, Issue 3, 2002, Pages 175-183

  Waterhouse, N J ^a   Trapani, J A ^a  

^a PETER MACCALLUM CANCER CENTRE   (Australia)

Author keywords

[No Author keywords available]

Indexed keywords

CALRETICULIN; CASPASE; CATHEPSIN D; DIPEPTIDYL PEPTIDASE I; GRANULYSIN; GRANZYME A; GRANZYME B; PERFORIN; GRANZYME; GZMB PROTEIN, MOUSE; MEMBRANE PROTEIN; PORE FORMING CYTOTOXIC PROTEIN; SERINE PROTEINASE; TUMOR NECROSIS FACTOR RECEPTOR;

APOPTOSIS; CELL DEATH; CELL GRANULE; CYTOTOXIC T LYMPHOCYTE; ENZYME ACTIVATION; ENZYME ACTIVITY; ENZYME INACTIVATION; HUMAN; KNOCKOUT MOUSE; NATURAL KILLER CELL; NONHUMAN; PRIORITY JOURNAL; REVIEW; SIGNAL TRANSDUCTION; TARGET CELL DESTRUCTION; ANIMAL; BIOLOGICAL MODEL; CYTOTOXICITY; IMMUNOLOGY; METABOLISM; MOUSE; PHYSIOLOGY;

ANIMAL; APOPTOSIS; CASPASES; CELL DEATH; CYTOTOXICITY, IMMUNOLOGIC; KILLER CELLS, NATURAL; MEMBRANE GLYCOPROTEINS; MICE; MODELS, IMMUNOLOGICAL; RECEPTORS, TUMOR NECROSIS FACTOR; SERINE ENDOPEPTIDASES; SIGNAL TRANSDUCTION; SUPPORT, NON-U.S. GOV'T; T-LYMPHOCYTES, CYTOTOXIC; ANIMALS; GRANZYMES; PORE FORMING CYTOTOXIC PROTEINS;

EID: 0035987541     PISSN: 00012815     EISSN: None     Source Type: Journal    
DOI: 10.1034/j.1399-0039.2002.590301.x     Document Type: Review

References (47)

1. Functional avidity of tumor antigen-specific CTL recognition directly correlates with the stability of MHC/peptide multimer binding to TCR
2. Microcinematographic and electron microscopic analysis of target cell lysis induced by cytotoxic T lymphocytes
3. Early steps in specific tumor cell lysis by sensitized mouse T lymphocytes. I. Resolution and characterization
4. Initiation of apoptosis by granzyme B requires direct cleavage of bid, but not direct granzyme B-mediated caspase activation
5. Assembly of two types of tubules with putative cytolytic function by cloned natural killer cells
6. Structural/functional similarity between proteins involved in complement- and cytotoxic T-lymphocyte-mediated cytolysis
7. Mechanisms of immune lysis. II. CTL-induced nuclear disintegration of the target begins within minutes of cell contact
8. Cytotoxic cell granule-mediated apoptosis. Perforin delivers granzyme b-serglycin complexes into target cells without plasma membrane pore formation
9. Cytosolic delivery of granzyme B by bacterial toxins: Evidence that endosomal disruption, in addition to transmembrane pore formation, is an important function of perforin
10. Exocytosis of cytolytic granules may not be required for target cell lysis by cytotoxic T-lymphocytes
11. Cytotoxicity mediated by T cells and natural killer cells is greatly impaired in perforin-deficient mice
12. Lymphocyte-mediated cytotoxicity: Two pathways and multiple effector molecules
13. Mechanisms mediating caspase activation in cell death
14. Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor
15. An APAF-1,cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9
16. Recruitment, activation and retention of caspases-9 and -3 by Apaf-1 apoptosome and associated XIAP complexes
17. Identification and molecular cloning of two novel receptors for the cytotoxic ligand TRAIL
18. Inhibition of death receptor signals by cellular FLIP
19. Antiapoptotic oncogenes prevent caspase-dependent and independent commitment for cell death
20. Inhibition of apoptosis and clonogenic survival of cells expressing crmA variants: Optimal caspase substrates are not necessarily optimal inhibitors
21. Caspase inhibitors
22. Conservation of baculovirus inhibitor of apoptosis repeat proteins (BIRPs) in viruses, nematodes, vertebrates and yeasts
23. Granzyme A is critical for recovery of mice from infection with the natural cytopathic viral pathogen, ectromelia
24. Granzyme B (GraB) autonomously crosses the cell membrane and perforin initiates apoptosis and GraB nuclear localization
25. Mannose 6-phosphate/insulin-like growth factor II receptor is a death receptor for granzyme B during cytotoxic T cell-induced apoptosis
26. A cytosolic granzyme B inhibitor related to the viral apoptotic regulator cytokine response modifier A is present in cytotoxic lymphocytes
27. The granzyme B inhibitor, protease inhibitor 9, is mainly expressed by dendritic cells and at immune-privileged sites
28. Blockade of the granzyme B/perforin pathway through overexpression of the serine protease inhibitor PI-9/SPI-6 constitutes a mechanism for immune escape by tumors
29. The cytotoxic cell protease granzyme B initiates apoptosis in a cell-free system by proteolytic processing and activation of the ICE/CED-3 family protease, CPP32, via a novel two-step mechanism
30. Granzyme B-mediated apoptosis proceeds predominantly through a Bc1-2-inhibitable mitochondrial pathway
31. Bc1-2 prevents apoptosis induced by perforin and granzyme B, but not that mediated by whole cytotoxic lymphocytes
32. Dependence of granzyme B-mediated cell death on a pathway regulated by Bc1-2 or its viral homolog, BHRF1
33. Cytotoxic lymphocytes require granzyme B for the rapid induction of DNA fragmentation and apoptosis in allogeneic target cells
34. Granzyme A is an interleukin 1 beta-converting enzyme
35. Granzyme A initiates an alternative pathway for granule-mediated apoptosis
36. Granzyme A loading induces rapid cytolysis and a novel form of DNA damage independently of caspase activation
37. Comparative modeling of amoebapores and granulysin based on the NK-lysin structure-structural and functional implications
38. A distinct pathway of cell-mediated apoptosis initiated by granulysin
39. Efficient nuclear targeting of granzyme B and the nuclear consequences of apoptosis induced by granzyme B and perforin are caspase-dependent, but cell death is caspase-independent
40. Cytochrome c maintains mitochondrial transmembrane potential and ATP generation after outer mitochondrial membrane permeabilization during the apoptotic process
41. A matrix-assisted laser desorption ionization post-source decay (MALDI-PSD) analysis of proteins released from isolated liver mitochondria treated with recombinant truncated Bid
42. Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins
43. HtrA2 promotes cell death through its serine protease activity and its ability to antagonize inhibitor of apoptosis proteins
44. The inhibitor of apoptosis protein-binding domain of Smac is not essential for its proapoptotic activity
45. DFF45/ICAD can be directly processed by granzyme B during the induction of apoptosis
46. Granzyme A and B-deficient killer lymphocytes are defective in eliciting DNA fragmentation but retain potent in vivo anti-tumor capacity
47. Lysosomal protease pathways to apoptosis. Cleavage of bid, not pro-caspases, is the most likely route