Caspases and T lymphocytes: A flip of the coin?

Immunological Reviews

Volumn 193, Issue , 2003, Pages 22-30

  Lakhani, Saquib ^a   Flavell, Richard A ^a  

^a YALE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

APOPTOTIC PROTEASE ACTIVATING FACTOR 1; CASPASE 3; CASPASE 8; ENZYME PRECURSOR; FAS ANTIGEN; INTERLEUKIN 1BETA CONVERTING ENZYME; PROTEIN BAK; PROTEIN BAX; PROTEIN BCL 2; PROTEIN BID; TUMOR NECROSIS FACTOR RECEPTOR;

APOPTOSIS; CELL DEATH; CELL STIMULATION; ENZYME ACTIVITY; IMMUNE RESPONSE; LYMPHOCYTE PROLIFERATION; PRIORITY JOURNAL; PROTEIN DOMAIN; REGULATORY MECHANISM; REVIEW; SIGNAL TRANSDUCTION; T LYMPHOCYTE;

ANIMALS; APOPTOSIS; CASPASES; ENZYME ACTIVATION; HUMANS; LYMPHOCYTE ACTIVATION; RECEPTORS, ANTIGEN, T-CELL; SIGNAL TRANSDUCTION; T-LYMPHOCYTES;

EID: 0037833743     PISSN: 01052896     EISSN: None     Source Type: Journal    
DOI: 10.1034/j.1600-065X.2003.00046.x     Document Type: Review

References (98)

1. Hildeman DA, et al. Activated T cell death in vivo mediated by proapoptotic bcl-2 family member bim. Immunity 2002;16:759-767.
2. Yuan J, Shaham S, Ledoux S, Ellis HM, Horvitz HR. The C. elegans cell death gene ced-3 encodes a protein similar to mammalian interleukin-1 beta-converting enzyme. Cell 1993;75:641-652.
3. Ellis HM, Horvitz HR. Genetic control of programmed cell death in the nematode C. elegans. Cell 1986;44:817-829.
4. Reddien PW, Cameron S, Horvitz HR. Phagocytosis promotes programmed cell death in C. elegans. Nature 2001;412:198-202.
5. Hengartner MO, Horvitz HR. C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2. Cell 1994;76:665-676.
6. Chinnaiyan AM, O'Rourke K, Lane BR, Dixit VM. Interaction of CED-4 with CED-3 and CED-9: a molecular framework for cell death. Science 1997;275:1122-1126.
7. Hengartner MO, Ellis RE, Horvitz HR. Caenorhabditis elegans gene ced-9 protects cells from programmed cell death. Nature 1992;356:494-499.
8. Conradt B, Horvitz HR. The C. elegans protein EGL-1 is required for programmed cell death and interacts with the Bcl-2-like protein CED-9. Cell 1998;93:519-529.
9. Xue D, Shaham S, Horvitz HR. The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease. Genes Dev 1996;10:1073-1083.
10. Thornberry NA, et al. A novel heterodimeric cysteine protease is required for interleukin-1 beta processing in monocytes. Nature 1992;356:768-774.
11. Wilson KP, et al. Structure and mechanism of interleukin-1 beta converting enzyme. Nature 1994;370:270-275.
12. Ramage P, et al. Expression, refolding, and autocatalytic proteolytic processing of the interleukin-1 beta-converting enzyme precursor. J Biol Chem 1995;270:9378-9383.
13. Kumar S. Mechanisms mediating caspase activation in cell death. Cell Death Differ 1999;6:1060-1066.
14. Meergans T, Hildebrandt AK, Horak D, Haenisch C, Wendel A. The short prodomain influences caspase-3 activation in HeLa cells. Biochem J 2000;349:135-140.
15. Yaoita Y. Inhibition of nuclear transport of caspase-7 by its prodomain. Biochem Biophys Res Commun 2002;291:79-84.
16. Cowling V, Downward J. Caspase-6 is the direct activator of caspase-8 in the cytochrome c-induced apoptosis pathway: absolute requirement for removal of caspase-6 prodomain. Cell Death Differ 2002;9:1046-1056.
17. Chinnaiyan AM, O'Rourke K, Tewari M, Dixit VM. FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis. Cell 1995;81:505-512.
18. Boldin MP, Varfolomeev EE, Pancer Z, Mett IL, Camonis JH, Wallach D. A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain. J Biol Chem 1995;270:7795-7798.
19. Kischkel FC, et al. Cytotoxicity-dependent APO-1 (Fas/CDgS)-associated proteins form a death-inducing signaling complex (DISC) with the receptor. EMBO J 1995;14:5579-5588.
20. Wang J, Chun HJ, Wong W, Spencer DM, Lenardo MJ. Caspase-10 is an initiator caspase in death receptor signaling. Proc Natl Acad Sci USA 2001;98:13884-13888.
21. Kischkel FC, et al. Death receptor recruitment of endogenous caspase-10 and apoptosis initiation in the absence of caspase-8. J Biol Chem 2001;276:46639-46646.
22. Muzio M, Stockwell BR, Stennicke HR, Salvesen GS, Dixit VM. An induced proximity model for caspase-8 activation. J Biol Chem 1998;273:2926-2930.
23. Scaffidi C, et al. Two CD95 (APO-1/Fas) signaling pathways. EMBO J 1998;17:1675-1687.
24. Woo M, et al. Essential contribution of caspase 3/CPP32 to apoptosis and its associated nuclear changes. Genes Dev 1998;12:806-819.
25. Lippke JA, Gu Y, Sarnecki C, Caron PR, Su MS. Identification and characterization of CPP32/Mch2 homolog 1, a novel cysteine protease similar to CPP32. J Biol Chem 1996;271:1825-1828.
26. Li H, Zhu H, Xu CJ, Yuan J. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell 1998;94:491-501.
27. Korsmeyer SJ, Wei MC, Saito M, Weiler S, Oh KJ, Schlesinger PH. Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c. Cell Death Differ 2000;7:1166-1173.
28. Lin X, Kim CN, Yang J, Jemmerson R, Wang X. Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c. Cell 1996;86:147-157.
29. Verhagen AM, et al. Identification of DIABLO, a mammalian protein that promotes apoptosis by binding to and antagonizing IAP proteins. Cell 2000;102:43-53.
30. Du C, Fang M, Li Y, Li L, Wang X. Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition. Cell 2000;102:33-42.
31. Hu Y, Ding L, Spencer DM, Nunez G. WD-40 repeat region regulates Apaf-1 self association and procaspase-9 activation. J Biol Chem 1998;273:33489-33494.
32. Qin H, Srinivasula SM, Wu G, Fernandes-Alnemri T, Alnemri ES, Shi Y. Structural basis of procaspase-9 recruitment by the apoptotic protease-activating factor 1. Nature 1999;399:549-557.
33. Saleh A, Srinivasula SM, Acharya S, Fishel R, Alnemri ES. Cytochrome c and dATP-mediated oligomerization of Apaf-1 is a prerequisite for procaspase-9 activation. J Biol Chem 1999;274:17941-17945.
34. Zou H, Li Y, Liu X, Wang X. An APAF-1 cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9. J Biol Chem 1999;274:11549-11556.
35. Li P, et al. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell 1997;91:479-489.
36. Acehan D, Jiang X, Morgan DG, Heuser JE, Wang X, Akey CW. Three-dimensional structure of the apoptosome: implications for assembly, procaspase-9 binding, and activation. Mol Cell 2002;9:423-432.
37. Rodriguez J, Lazebnik Y. Caspase-9 and APAF-1 form an active holoenzyme. Genes Dev 1999;13:3179-3184.
38. Stennicke HR, Deveraux QL, Humke EW, Reed JC, Dixit VM, Salvesen GS. Caspase-9 can be activated without proteolytic processing. J Biol Chem 1999;274:8359-8362.
39. Varfolomeev EE, et al. Targeted disruption of the mouse Caspase 8 gene ablates cell death induction by the TNF receptors, Fas/Apol, and DR3 and is lethal prenatally. Immunity 1998;9:267-276.
40. Yeh WC, et al. FADD: essential for embryo development and signaling from some, but not all, inducers of apoptosis. Science 1998;279:1954-1958.
41. Zhang J, Cado D, Chen A, Kabra NH, Winoto A. Fas-mediated apoptosis and activation-induced T-cell proliferation are defective in mice lacking FADD/Mortl. Nature 1998;392:296-300.
42. Li K, et al. Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis. Cell 2000;101:389-399.
43. Kuida K, et al. Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9. Cell 1998;94:325-337.
44. Hakem R, et al. Differential requirement for caspase 9 in apoptotic pathways in vivo. Cell 1998;94:339-352.
45. Marsden VS, et al. Apoptosis initiated by Bcl-2-regulated caspase activation independently of the cytochrome c/Apaf-1/caspase-9 apoptosome. Nature 2002;419:634-637.
46. Zheng TS, et al. Deficiency in caspase-9 or caspase-3 induces compensatory caspase activation. Nat Med 2000;6:1241-1247.
47. Eischen CM, et al. ZAP-70 tyrosine kinase is required for the up-regulation of Fas ligand in activation-induced T cell apoptosis. J Immunol 1997;159:1135-1139.
48. Gonzalez-Garcia A, R-Borlado L, Leonardo E, Merida I, Martinez AC, Carrera AC. Lck is necessary and sufficient for Fas-ligand expression and apoptotic cell death in mature cycling T cells. J Immunol 1997;158:4104-4112.
49. Miller AT, Berg LJ. Defective Fas ligand expression and activation-induced cell death in the absence of IL-2-inducible T cell kinase. J Immunol 2002;168:2163-2172.
50. Tanaka N, et al. Differential involvement of p38 mitogen-activated protein kinase kinases MKK3 and MKK6 in T-cell apoptosis. EMBO Rep 2002;3:785-791.
51. Dong C, Yang DD, Wysk M, Whitmarsh AJ, Davis RJ, Flavell RA. Defective T cell differentiation in the absence of Jnk1. Science 1998;282:2092-2095.
52. Sabapathy K, et al. JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development. Curr Biol 1999;9:116-125.
53. Zhang J, et al. Regulation of fas ligand expression during activation-induced cell death in T cells by p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase. J Exp Med 2000;191:1017-1030.
54. Zhu L, Yu X, Akatsuka Y, Cooper JA, Anasetti C. Role of mitogen-activated protein kinases in activation-induced apoptosis of T cells. Immunology 1999;97:26-35.
55. + T cells. Annu Rev Immunol 1994;12:635-673.
56. Smith KA. Interleukin-2: inception, impact, and implications. Science 1988;240:1169-1176.
57. Lenardo MJ, Interleukin-2 programs mouse alpha beta T lymphocytes for apoptosis. Nature 1991;353:858-861.
58. Sadlack B, Merz H, Schorle H, Schimpl A, Feller AC, Horak I. Ulcerative colitis-like disease in mice with a disrupted interleukin-2 gene. Cell 1993;75:253-261.
59. Kneitz B, Herrmann T, Yonehara S, Schimpl A. Normal clonal expansion but impaired Fas-mediated cell death and anergy induction in interleukin-2-deficient mice. Eur J Immunol 1995;25:2572-2577.
60. Van Parijs L, Biuckians A, Ibragimov A, Alt FW, Willerford DM, Abbas AK. Functional responses and apoptosis of CD25 (IL-2R alpha)-deficient T cells expressing a transgenic antigen receptor. J Immunol 1997;158:3738-3745.
61. van Parijs L, Refaeli Y, Lord JD, Nelson BH, Abbas AK, Baltimore D. Uncoupling IL-2 signals that regulate T cell proliferation, survival, and Fas-mediated activation-induced cell death. Immunity 1999;11:281-288.
62. Refaeli Y, Van Parijs L, Alexander SI, Abbas AK. Interferon gamma is required for activation-induced death of T lymphocytes. J Exp Med 2002;196:999-1005.
63. Refaeli Y, Van Parijs L, London CA, Tschopp J, Abbas AK. Biochemical mechanisms of IL-2-regulated Fas-mediated T cell apoptosis. Immunity 1998;8:615-623.
64. Thome M, et al. Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptors. Nature 1997;386:517-521.
65. Hu S, Vincenz C, Bullet M, Dixit VM. A novel family of viral death effector domain-containing molecules that inhibit both CD-95- and tumor necrosis factor receptor-1-induced apoptosis. J Biol Chem 1997;272:9621-9624.
66. Bertin J, et al. Death effector domain-containing herpesvirus and poxvirus proteins inhibit both Fas- and TNFR1-induced apoptosis. Proc Natl Acad Sci USA 1997;94:1172-1176.
67. Thome M, Tschopp J. Regulation of lymphocyte proliferation and death by FLIP. Nat Rev Immunol 2001;1:50-58.
68. Han DK, et al. MRIT, a novel death-effector domain-containing protein, interacts with caspases and BclXL and initiates cell death. Proc Natl Acad Sci USA 1997;94:11333-11338.
69. Irmler M, et al. Inhibition of death receptor signals by cellular FLIP. Nature 1997;388:190-195.
70. Srinivasula SM, et al. FLAME-1, a novel FADD-like anti-apoptotic molecule that regulates Fas/TNFR1-induced apoptosis. J Biol Chem 1997;272:18542-18545.
71. Krueger A, Schmitz I, Baumann S, Krammer PH, Kirchhoff S. Cellular FLICE-inhibitory protein splice variants inhibit different steps of caspase-8 activation at the CD95 death-inducing signaling complex. J Biol Chem 2001;276:20633-20640.
72. Shu HB, Halpin DR, Goeddel DV. Casper is a FADD- and caspase-related inducer of apoptosis. Immunity 1997;6:751-763.
73. Yeh WC, et al. Requirement for Casper (c-FLIP) in regulation of death receptor-induced apoptosis and embryonic development. Immunity 2000;12:633-642.
74. Nagata S. Human autoimmune lymphoproliferative syndrome, a defect in the apoptosis-inducing Fas receptor: a lesson from the mouse model. J Hum Genet 1998;43:2-8.
75. Cohen PL, Eisenberg RA. Lpr and gld: single gene models of systemic autoimmunity and lymphoproliferative disease. Annu Rev Immunol 1991;9:243-269.
76. Adachi M, et al. Targeted mutation in the Fas gene causes hyperplasia in peripheral lymphoid organs and liver. Nat Genet 1995;11:294-300.
77. Takahashi T, et al. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 1994;76:969-976.
78. Russell JH, Rush B, Weaver C, Wang R. Mature T cells of autoimmune lpr/lpr mice have a defect in antigen-stimulated suicide. Proc Natl Acid Sci USA 1993;90:4409-4413.
79. Canale VC, Smith CH. Chronic lymphadenopathy simulating malignant lymphoma. J Pediatr 1967;70:891-899.
80. Sneller MC, et al. A novel lymphoproliferative/autoimmune syndrome resembling murine lpr/gld disease. J Clin Invest 1992;90:334-341.
81. Straus SE, Sneller M, Lenardo MJ, Puck JM, Strober W. An inherited disorder of lymphocyte apoptosis: the autoimmune lymphoproliferative syndrome. Ann Intern Med 1999;130:591-601.
82. Fisher GH, et al. Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome. Cell 1995;81:935-946.
83. Rieux-Laucat F, et al. Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity. Science 1995;268:1347-1349.
84. Wang J, et al. Inherited human Caspase 10 mutations underlie defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoproliferative syndrome type II. Cell 1999;98:47-58.
85. Wu J, Wilson J, He J, Xiang L, Schur PH, Mountz JD Fas ligand mutation in a patient with systemic lupus erythematosus and lymphoproliferative disease. J Clin Invest 1996;98:1107-1113.
86. Vidal S, Kono DH, Theofilopoulos AN. Loci predisposing to autoimmunity in MRL-Fas lpr and C57BL/6-Faslpr mice. J Clin Invest 1998;101:696-702.
87. Chun HJ, et al. Pleiotropic defects in lymphocyte activation caused by caspase-8 mutations lead to human immunodeficiency. Nature 2002;419:395-399.
88. Alderson MR, et al. Fas transduces activation signals in normal human T lymphocytes. J Exp Med 1993;178:2231-2235.
89. Miossec C, Dutilleul V, Fassy F, Diu-Hercend A. Evidence for CPP32 activation in the absence of apoptosis during T lymphocyte stimulation. J Biol Chem 1997;272:13459-13462.
90. Wilhelm S, Wagner H, Hacker G. Activation of caspase-3-like enzymes in non-apoptoric T cells. Eur J Immunol 1998;28:891-900.
91. Hueber AO, Zornig M, Bernard AM, Chautan M, Evan G. A dominant negative Fas-associated death domain protein mutant inhibits proliferation and leads to impaired calcium mobilization in both T-cells and fibroblasts. J Biol Chem 2000;275:10453-10462.
92. Newton K, Harris AW, Bath ML, Smith KG, Strasser A. A dominant interfering mutant of FADD/MORT1 enhances deletion of autoreactive thymocytes and inhibits proliferation of mature T lymphocytes. EMBO J 1998;17:706-718.
93. Newton K, Kurts C, Harris AW, Strasser A. Effects of a dominant interfering mutant of FADD on signal transduction in activated T cells. Curr Biol 2001;11:273-276.
94. Adam A, Cohen LY, Aouad S, Sekaly RP. Early activation of caspases during T lymphocyte stimulation results in selective substrate cleavage in nonapoptotic cells. J Exp Med 1999;190:1879-1890.
95. Kennedy NJ, Kataoka T, Tschopp J, Budd RC. Caspase activation is required for T cell proliferation. J Exp Med 1999;190:1891-1896.
96. Micheau O, et al. The long form of FLIP is an activator of caspase-8 at the Fas death-inducing signaling complex. J Biol Chem 2002;277:45162-45171.
97. Kataoka T, et al. The caspase-8 inhibitor FLIP promotes activation of NF-kappaB and Erk signaling pathways. Curr Biol 2000;10:640-648.
98. Lens SM, et al. The caspase 8 inhibitor c-FLIP (L) modulates T-cell receptor-induced proliferation but not activation-induced cell death of lymphocytes. Mol Cell Biol 2002;22:5419-5433.