Apoptosis and the maintenance of homoeostasis in the immune system

Current Opinion in Immunology

Volumn 8, Issue 2, 1996, Pages 245-254

  Osborne, Barbara A ^a  

^a UNIVERSITY OF MASSACHUSETTS   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

FAS ANTIGEN;

APOPTOSIS; B LYMPHOCYTE; HOMEOSTASIS; HUMAN; IMMUNE SYSTEM; MOUSE; NONHUMAN; REVIEW; SIGNAL TRANSDUCTION; T LYMPHOCYTE;

EID: 0029993331     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(96)80063-X     Document Type: Article

References (89)

1. Nossal GJV: Negative selection of lymphocytes. Cell 1994, 76:229-239.
2. Smith CA, Williams G, Kingston R, Jenkinson EJ, Owen JT: Antibodies to CD3/T-cell receptor complex induces death by apoptosis in immature T cells in thymic culture. Nature 1989, 337:181-183.
3. MacDonald HR, Lees RK: Programmed death of autoreactive thymocytes. Nature 1990, 343:624-646.
4. Hartley SB, Cooke MP, Fulcher DA, Harris AW, Cory S, Basten A, Goodnow CC: Elimination of self-reactive B lymphocytes proceeds in two stages: arrested development and cell death. Cell 1993, 72:325-335.
5. Surh CD, Sprent J: T-cell apoptosis detected in situ during positive and negative selection in the thymus. Nature 1994, 372:100-103. This paper conclusively demonstrates that most of the T cells in the thymus die before leaving the thymus. The data also indicate that the majority of cells that die in thymus die as a result of failure of positive selection, or death by neglect.
6. Allen PM: Peptides in positive and negative selection: a delicate balance. Cell 1994, 76:593-596.
7. Sprent J, Lo D, Gao EK, Ron Y: T cell selection in the thymus. Immunol Rev 1988, 101:172-190.
8. Zacharchuk CM, Mercep M, Ashwell JD: Programmed T lymphocyte death: cell activation- and steroid-induced pathways are mutually antagonistic. J Immunol 1990, 145:4037-4045.
9. Iwata M, Hanaoka S, Sato K: Rescue of thymocytes and T cell hybridomas from glucocorticoid-induced apoptosis by stimulation via the T cell receptor/CD3 complex: a possible in vitro model for positive selection of the T cell repertoire. Eur J Immunol 1991, 21:643-648.
10. Wyllie AH: Glucocorticold induced thymocyte apoptosis is associated with endogenous endonuclease activation. Nature 1980, 284:555-556.
11. ••].
12. + cells.
13. + thymocytes. J Immunol 1993, 151:1868-1880.
14. + thymocytes by T-cell receptor-induced apoptosis requires a costimulatory signal that can be provided by CD28. J Exp Med 1994, 179:709-713.
15. Foy TM, Page DM, Waldschmidt TJ, Schoneveld A, Laman JD, Masters SR, Tygrett L, Ledbetter JA, Aruffo A, Claassen E et al.: An essential role for gp39, the ligand for CD40, in thymic selection. J Exp Med 1995, 182:1377-1388.
16. Lowe SW, Schmidtt EM, Smith SW, Osborne BA, Jacks T: p53 is required for radiation-induced apoptosis in mouse thymocytes. Nature 1993, 362:847-849.
17. Clarke AR, Purdie CA, Harrison DJ, Morris RG, Bird CC, Hooper ML, Wyllie AH. Thymocyte apoptosis induced by p53-dependent and independent pathways. Nature 1993, 362:849-852.
18. Woronicz JD, Calnan B, Ngo V, Winolo A: Requirement for the orphan steroid receptor Nur77 in apoptosis of T cell hybridomas. Nature 1994, 367:277-281.
19. Liu ZG, Smith SW, McLauglin KA, Schwartz LM, Osborne BA: Apoptotic signals delivered through the T-cell receptor require the immediate-early gene nur77. Nature 1994, 367:281-284.
20. Lee SL, Wesselachmidt RL, Linette GP, Kanagawa O, Russell JH, Milbrandt J: Unimpaired thymic and peripheral T cell death in mice lacking the nuclear receptor NGFI-B (Nur77). Science 1995, 269:532-535. This paper suggests that targeted deletion of the nur77 gene has no effect on either peripheral or thymic cell death. It is important to note, however, that it does not rule out the possibility that other closely related members of the nuclear hormone receptor superfamily may substitute for nur77 expression.
21. •], this mouse exhibits defects in negative selection.
22. Dieken ES, Miesfeld RL: Transcriptional transactivation functions localized to the glucocorticoid receptor N terminus are necessary for steroid induction of lymphocyte apoptosis. Mol Cell Biol 1992, 12:589-587.
23. Norvell A, Mandik L, Monroe JG: Engagement of the antigen-receptor on immature murine B lymphocytes results in death by apoptosis. J Immunol 1995, 154:4404-4413. This paper is the first to show that purified immature B cells isolated from bone marrow may be induced to die by cross-linking of the antigen receptor. The paper also provides a useful for method purifying immature B cells, allowing future experiments to address the molecular mechanisms by which immature B-cell populations undergo apoptosis.
24. ••].
25. ••].
26. ••] published together, provide the first conclusive evidence that activation-induced death in T cell hybridomas, Jurkat cells and non-transformed T cells occurs by Fas/FasL interaction. In addition, the data in these papers demonstrate that Fas-induced death can occur either by suicide or fratricide.
27. 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 Acad Sci USA 1993, 90:4409-4413.
28. Russell JH, Wang R: Autoimmune gld mutation uncouples suicide and cytokine/proliferation pathways in activated mature T cells. Eur J Immunol 1993, 23:2379-2382.
29. Adachi M, Suematsu S, Kondo T, Ogasawara J, Tanaka T, Yoshida N, Nagata S: Targeted mutation in the Fas gene cause hyperplasia in the peripheral lymphoid organs and liver. Nature Genetics 1995, 11:294-300.
30. Adachi M, Suematsu S, Suda T, Watanabe D, Fukuyama H, Ogasawara J, Tanaka T, Yoshida N, Nagata S: Enhanced and accelerated lymphoproliferation in Fas-null mice. Proc Natl Acad Sci USA 1996, in press. The targeted deletion of Fas provides clear evidence that Fas does not play a role in thymic deletion. The data also demonstrate that deletion of the Fas gene has a phenotype more severe than that observed in lpr/lpr mice.
31. + cells in lpr mice.
32. Giese T, Davidson WF: Chronic treatment of C3H-lpr/lpr and C3H-gld/gld mice with anti-CD8 monoclonal antibody prevents the accumulation of double negative T cells but not autoantibody production. J Immunol 1994, 152:2000-2010.
33. Watanabe D, Suda T, Nagata S: Expression of Fas in B cells of the mouse germinal center and Fas-dependent killing of activated B cells. Int Immunol 1995, 12:in press.
34. + T cells, and that this elimination depends upon Fas-FasL interaction. When these experiments are performed on an lpr background, the B cells proliferate and make antibody.
35. Rothstein TL, Wang MM, Panka, DJ, Foote LC, Wang Z, Stanger B, Cul H, Ju S-T, Marshak-Rothstein A: Protection against Fas-dependent Th1-mediated apoptosis by antigen receptor engagement in B cells. Nature 1995, 374:163-165. This paper provides convincing evidence that CD40 cross-linking makes a B cell susceptible to Fas-induced apoptosis unless the B cell is also stimulated through the Ig receptor. The data presented here suggest a mechanism by which activated bystander B cells may be eliminated.
36. ••].
37. ••] demonstrate that antigen-specific B cells in germinal centers undergo apoptosis following exposure to soluble antigen, and that this may be the mechanism that prevents the activation of autoreactive B cells that might develop following somatic hypermutation.
38. ••] by demonstrating that the cell death observed in germinal center B cells following exposure to antigen does not involve Fas/FasL interaction.
39. Singer GG, Abbas AK: The Fas antigen is involved in peripheral but not thymic deletion of T lymphocytes in T cell receptor transgenic mice. Immunity 1994, 1:365-371.
40. Rathmell JC, Goodnow CC: Effects of the lpr mutation on elimination and inactivation of self-reactive B cells. J Immunol 1994, 153:2831-2842. This paper provided the first evidence that Fas mediates the elimination of activated mature B cells in much the same fashion as the Fas pathway eliminates activated peripheral T cells.
41. Dhein J, Daniel PT, Trauth BC, Oehm A, Möller P, Krammer PH: Induction of apoptosis by monoclonal antibody anti-APO-1 class switch variants is dependent on cross-linking of APO-1 cell surface antigens. J Immunol 1992, 149:3166-3173.
42. Nagata S, Golstein P: The Fas death factor. Science 1995, 267:1449-1456.
43. ••].
44. Yuan J: Molecular control of life and death. Curr Opin Cell Biol 1995, 7:211-214.
45. ••].
46. ••].
47. ••].
48. Hsu H, Ziong J, Goeddel DV: The TNF receptor 1-associated protein TRADD signals cell death and NF-B activation. Cell 1995, 81:496-504.
49. Berke G: The CTLs kiss of death. Cell 1995, 81:9-12.
50. cdc2 activation required for apoptosis. Science 1994, 263:1143-1146.
51. Chen G, Shi L, Litchfield DW, Greenberg AH: Rescue from granzymeB-induced apoptosis by Wee1 kinase. J Exp Med 1995, 181:2295-2300. This paper extends earlier elegant studies from this group which demonstrated a requirement for activation of cdc2 during granzyme-B-induced apoptosis in target cells. The current paper presents evidence that expression of Weel kinase, a kinase that inactivates cdc2, renders cells resistant to granzyme-B-induced apoptosis.
52. Darmon AJ, Nicholson DW, Bleackley RC: Activation of the apoptotic protease CPP32 by cytotoxic T-cell-derived granzyme B. Nature 1995, 377:446-448. This is the first report of the activation of an ICE family member by granzyme B, and suggests an important role for ICE family members in CTL-induced death.
53. Kagi D, Lederman B, Brki K, Seiler P, Odermatt B, Olsen KJ, Podack ER, Zinkernagel RM, Hengartner H: Cytotoxicity mediated by T cells and natural killer tells is greatly impaired in perforin-defident mice. Nature 1994, 369:31-37.
54. Heusel JW, Wesselschmidt RL, Shresta S, Russell JH, Ley TJ: Cytotoxic lymphocytes require granzyme B for the rapid Induction of DNA fragmentation and apoptosis in allogeneic target cells. Cell 1994, 76:977-987.
55. Lowin B, Hahne M, Mattmann C, Tschopp J: Cytolytlc T-cell cytotoxicity is mediated through perform and Fas lytic pathways. Nature 1994, 370:650-652.
56. 2+-independent T cell-mediated cytotoxicity. J Exp Med 1993, 177:195-200.
57. Ramsdell F, Seaman MS, Miller RE, Tough TW, Alderson MR, Lynch DH: gld/gld mice are unable to express a functional ligand for Fas. Eur J Immunol 1994, 24:928-933.
58. Tsujimoto Y, Finger LR, Yunis J, Nowell PC, Croce CM: Cloning of the chromosome breakpoint of neoplastic B cells with the t(14:18) translocation. Science 1984, 226:1097-1099.
59. Vaux DL, Cory S, Adams JM: Bcl-2 gene promotes haemopoietic cell survival and co-operates with c-myc to immortalize pre-B cells. Nature 1988, 335:440-442.
60. Strasser A: Life and death during lymphocyte development and function: evidence for two distinct killing mechanisms. Curr Opin Immunol 1995, 7:228-234.
61. Linette G, Korsmeyer S: Differentiation and cell death: lessons from the immune system. Curr Opin Cell Biol 1994, 6:809-815.
62. Cory S: BCL-2 family and lymphocyte survival. Annu Rev Immunol 1995, 13:513-543.
63. + stage during positive selection and promotes thymocyte differentiation at several control points. Immunity 1994, 1:197-205.
64. Sentman CL, Shutter JR, Hockenberry D, Kanagawa O, Korsmeyer SJ: Bcl-2 inhibits multiple forms of apoptosis but not negative selection in thymocytes. Cell 1991, 67:879-868.
65. Strasser A, Harris AW, Cory S: Bcl-2 transgene inhibits T cell death and perturbs thymic self-censorship. Cell 1991, 67:889-899.
66. Veis DJ, Sorenson CM, Shutter JR, Korsmeyer SJ: Bcl-2-deficient mice demonstrate fulminant lymphoid apoptosis, polycystic kidneys, and hypopigmented hair. Cell 1993, 75:229-240.
67. Oltvai ZN, Milliman CL, Korsmeyer SJ: Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death. Cell 1993, 74:609-619.
68. Knudson CM, Tung KSK, Tourtellotte WG, Brown GAJ, Korsmeyer SJ: Bax-deficient mice with lymphoid hyperplasia and male germ cell death. Science 1995, 270:96-93. This paper reports the derivation of mice deficient for Bax, the partner of Bcl-2 reported to counteract the survival effects of Bcl-2. As might be expected, mice that lack Bax, an apoptosis-promoting gene, have hyperplasia of both T-cell and B-cell compartments.
69. Boise LH, Gonzalez-Garcia M, Postema CE, Ding L, Lindsten T, Turka LA, Mao X, Nunez G, Thompson C. Bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death. Cell 1993, 74:597-608.
70. Motoyama N, Wang F, Roth KA, Sawa H, Nakayama K, Nakayama K, Negishi I, Senju S, Zhang Q, Fujii S, Loh DY: Massive cell death of immature hematopoletic cells and neurons in Bcl-x-deficient mice. Science 1995, 267:1506-1510. The data in this paper demonstrate that deletion of Bcl-x results in embryonic death at approximately day E13. These embryos display massive cell death in neuronal cells and hematopoietic cells in the liver. Chimeras of such mice with deletion of Bcl-x in the lymphoid lineage exhibit a shortened life span of immature lymphocytes and diminished ability of these cells to mature.
71. L and Bcl-2, displaces Bax and promotes cell death. Cell 1995, 80:285-291.
72. Sedlak TW, Oltavi ZN, Yang E, Wang K, Boise LH, Thompson CB, Korsmeyer SJ: Multiple Bcl-2 family members demonstrate selective dimerizations with Bax. Proc Natl Acad Sci USA 1995, 92:7834-7838.
73. Zamzami N, Marchetti P, Castedo M, Zanin C, Vayssièrs, Petir PX, Kroemer G: Reduction in mitochondrial potential constitutes an early irreversible step of programmed lymphocyte death in vivo. J Exp Med 1995, 181:1661-1672.
74. Osborne BA, Smith SW, McLauglin KA, Grimm L, Kallinch T, Schwartz LM: Identification of genes induced during apoptosis in T lymphocytes. Immunol Rev 1994, 142:301-320.
75. Hockenberry DM, Oltvai ZN, Yin XM, Milliman CL, Korameyer SJ. Bcl-2 functions in an antioxidant pathway to prevent apoptosis. Cell 1993, 75:241-251.
76. Gulbins E, Bissonette R, Mahboubi A, Martin S, Nishioka W, Brunner T, Baier G, Baier-Bitterlich G, Byrd C, Lang F et al.: FAS-induced apoptosis is mediated via a ceramide-initiated RAS signaling pathway. Immunity 1995, 2:314-351.
77. Sarin A, Adams DH, Henkart PA: Protease inhibitors selectively block T-cell receptor-triggered programmed cell death in a murine T cell hybridoma and activated peripheral T cells. J Exp Med 1993, 178:1693-1700.
78. Sarin A, Nakajima H, Henkart PA: A protease dependent TCP-induced death pathway in mature lymphocytes. J Immunol 1995, 154:5806-5812.
79. Kuida K, Lippke JA, Ku G, Harding MW, Livingston DJ, Su MS, Flavell RA: Altered cytokine export and apoptosis in mice deficient in interleukin-1 beta converting enzyme. Science 1995, 267:2000-2003.
80. •].
81. •].
82. •] provide evidence for the involvement of ICE family members in Fas-mediated apoptosis. Although some disagreement exist among the authors as to the involvement of ICE or CPP32 or new family members such as ICE-LAP3, it appears clear that these proteases play an important role in the Fas-mediated death of T cells.
83. ••].
84. •] demonstrate that mutations in Fas cause similar disease in humans as that observed in lpr/lpr mice.
85. •].
86. •] make the interesting observation that Fas-FasL interactions are important in preventing tissue damage as a result of inflammation in certain delicate tissues such as the eye and testis.
87. Gougeon ML, Laurent CA, Hovanessian AG, Montagnier L: Direct and indirect mechanisms mediating apoptosis during HIV infection: contribution to in vivo CD4 T cell depletion. Semin Immunol 1993, 5:187-194.
88. Ameisen JC, Estaquier J, Idziorek T, De Bels F: The relevance of apoptosis to AIDS pathogenesis. Trends Cell Biol 1995, 5:27-32.
89. Finkel TH, Tudor-Williams G, Banda NK, Cotton MF, Curiel T, Monks C, Baba TW, Ruprecht RM, Kupfer A: Apoptosis occurs predominately in bystander cells and not in productively infected cells of HIV- and SIV-infected lymph nodes. Nat Med 1995, 1:129-134.