Abstract
The pathogenesis of systemic lupus erythematosus (SLE) is multifactorial and multi-genetic. Chronic inflammation associated with lupus is thought to be due to loss of self-tolerance due to molecular mimicry, environment trigger, hormonal factors or apoptosis defects. Defects in apoptosis will be the focus of this chapter. Defects in apoptosis can lead to abnormal clonal deletion of autoreactive cells or failure to downmodulate an inflammatory response. Although the Fas death domain family of molecules are the primary pathway for elimination of inflammatory cells, defects in these death domain molecules are rarely observed in lupus and lupus-like syndromes. Patients with autoimmune-lymphoproliferative (ALPS) syndrome disease have defects in Fas, and we have reported one patient with SLE that exhibits a mutation of Fas ligand. Other death domain family molecules such as death receptor 3 (DR3), DR4, DRS, Fas ligand 2 (FasL2) have not been studied in SLE. Also, there are signaling pathways for apoptosis including Fas-associated protein with death domain (FADD), tumor necrosis factor receptor-1 associated death domain (TRADD), FADD-like interleukin-113 converting enzyme (FLICE) which are important in apoptosis signaling. The bc1-2 family modulate apoptosis, and have been reported to be abnormal in human autoimmune disease. Soluble inhibitors of Fas apoptosis including a soluble form of Fas which lacks the transmembrane exon are elevated in SLE patients. Different genetic and environmental factors are proposed to interfere with apoptosis and clearance of inflammatory cells at several levels leading to the cellular defects of T cell dysfunction and B cell hyperactivity observed in patients with SLE.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Watanabe-Fukunaga R, Brannan CI, Copeland NG, Jenkins NA, Nagata S (1992) Lym-phoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature 356: 314–317
Wu J, Zhou T, He J, Mountz JD.(1993) Murine autoimmune disease due to integration of an endogenous retrovirus in an apoptosis gene. J Exp Med 178: 461–468
Adachi M, Watanabe-Fukunaga R, Nagata S (1993) Aberrant transcription caused by the insertion of an early transposable element in an intron of the Fas antigen gene of lpr mice. Proc Natl Acad Sci USA 90: 1756–1760
Chu J-L, Drappa J, Parnassa AP, Elkon KB (1993) The defect in Fas mRNA expression in MRL/lpr mice is associated with insertion of the retrotransposon, ETn. J Exp Med 178: 723–732
Nagata S (1994) Mutations in the Fas antigen gene in 1pr mice. Sem Immunol 6: 3–26
Takahashi T, Tanaka M, Brannan CI, Jenkins NA, Copeland NG, Suda T, Nagata S. (1994) Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 76: 969–976
Lynch DH, Watson ML, Alderson MR, Baum PR, Miller RE, Tough T, Gibson M, Davis-Smith T, Smith CA, Hunter K, Bhat D, Din W, Goodwin RG, Seldin MF (1994) The mouse Fas-ligand gene is mutated in gld mice and is part of a TNF family gene cluster. Immunity 1: 131–136
Nagata S, Suda T (1995) Fas and Fas ligand: lpr and gld mutations. Immunol Today 16: 39–43
Fisher GH, Rosenberg FJ, Straus SE, Dale L, Middleton LA, Lin AY, Strober W, Leonardo MJ, Puck JM (1995) Dominant interfering Fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome. Cell 81: 935–946
Rieux-Laucat F, LeDeist F, Hivroz C, Roberts IA, Fritz S, Pearlstein GR, Puck JM, Leonardo MJ, Straus SE (1995) Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity. Science 263: 1347–1349
Fuss IJ, Strober W, Dale JK, Stüber MW, Middleton MA, Choi Y, Fleisher TA, Lim MS, Jaffe ES, Puck JM (1997) Characteristic T helper 2 T cell cytokine abnormalities in autoimmune lymphoproliferative syndrome, a syndrome marked by defective apoptosis and humoral autoimmunity. J Immunol 158: 1912–1618
Sneller MC, Wang J, Dale JK, et al (1997) Clinical, immunologic, and genetic features of an autoimmune lymphoproliferative syndrome associated with abnormal lymphocyte apoptosis. Blood 89: 1341–1348
Drappa J, Vaishnaw AK, Sullivan KE, Chu IL, Elkon KB (1996) Fas gene mutations in the Canale-Smith syndrome, an inherited lymphoproliferative disorder associated with autoimmunity. New Engl J Med 335: 1643–1649
Wu J, Wilson J, He J, Xiang L, Schur PH, Mountz JD (1996) Fas ligand mutation in a patient with systemic lupus erythematosus and lymphoproliferative disease. J Clin Invest 98: 1107–1113
Mountz JD, Wu J, Cheng J, Zhou T (1994) Autoimmune disease. A problem of defective apoptosis. Arthritis Rheum 37: 1415–1420
Elkon KB (1994) Apoptosis in SLE — too little or too much? Clin Exp Rheumatol 12: 553–559
Ravirajan CT. Sarraf CE. Anilkumar TV. Golding MC. Alison MR. Isenberg DA (1996) An analysis of apoptosis in lymphoid organs and lupus disease in murine systemic lupus erythematosus (SLE). Clin Exp Immunol 105: 306–312
Richardson BC. Yung RL. Johnson KJ. Rowse PE. Lalwani ND (1996) Monocyte apoptosis in patients with active lupus. Arthritis Rheum 39: 1432–1444
Rose LM. Latchman DS. Isenberg DA (1997) Apoptosis in peripheral lymphocytes in systemic lupus erythematosus: a review. Br J Rheum 36: 158–163
Grone HJ (1996) Systemic lupus erythematosus and antiphospholipid syndrome. Pathologe 17: 405–416
Casciola-Rosen L, Rosen A, Petri M, Schlissel M (1996) Surface blebs on apoptotic cells are sites of enhanced procoagulant activity: implications for coagulation events and antigenic spread in systemic lupus erythematosus. Proc Natl Acad Sci USA 93: 1624–1629
Nakamura N, Kuragaki C, Shidara Y, Yamaji K, Wada Y (1995) Antibody to annexin V has anti-phospholipid and lupus anticoagulant properties. Am J Hemat 49: 347–348
Rosen A, Casciola-Rosen L, Ahearn J (1995) Novel packages of viral and self-antigens are generated during apoptosis. J Exp Med 181: 1557–1561
Casciola-Rosen L, Rosen A (1997) Ultraviolet light-induced keratinocyte apoptosis: a potential mechanism for the induction of skin lesions and autoantibody production in LE. Lupus 6: 175–180
Van Bruggen MC, Kramers C, Berden JH (1996) Autoimmunity against nucleosomes and lupus nephritis. Annales de Medecine Interne 147: 485–489
Krieg AM (1995) CpG DNA: a pathogenic factor in systemic lupus erythematosus? J Clin Immunol 15: 284–292
Newkirk MM, Shiroky JB, Johnson N, Danoff D, Isenberg DA, Shustik C, Pearson GR (1996) Rheumatic disease patients, prone to Sjogren’s syndrome and/or lymphoma, mount an antibody response to BHRF1, the Epstein-Barr viral homologue of BCL-2. Brit J Rheum 35: 1075–1081
Utz PJ, Hottelet M, Schur PH, Anderson P (1997) Proteins phosphorylated during stress-induced apoptosis are common targets for autoantibody production in patients with systemic lupus erythematosus. J Exp Med 185: 843–854
Kovacs B, Patel A, Hershey JN, Dennis GJ, Kirschfink M, Tsokos GC (1997) Antibodies against p53 in sera from patients with systemic lupus erythematosus and other rheumatic diseases. Arthritis Rheum 40: 980–982, 1997
Wu J, Edberg JC, Redecha PB, Bansal V, Guyre PM, Coleman K, Salmon JE, Kimberly RP (1997) A novel polymorphism of FcyRIIIa (CD16) alters receptor function and predisposes to autoimmune disease. J Clin Invest 100: 1059–1070
Chan EY, Ko SC, Lau CS (1997) Increased rate of apoptosis and decreased expression of bd-2 protein in peripheral blood lymphocytes from patients with active systemic lupus erythematosus. Asian Pac J Allergy Immunol 15: 3–7
Rose LM, Latchman DS, Isenberg DA (1995) Bc1–2 expression is unaltered in unfractionated peripheral blood mononuclear cells in patients with systemic lupus erythematosus. Brit J Rheum 34: 316–320
Rose LM, Latchman DS, Isenberg DA (1994) Bc1–2 and Fas, molecules which influence apoptosis. A possible role in systemic lupus erythematosus? Autoimmunity 17: 271–278
Ohsako S, Hara M, Harigai M, Fukasawa C, Kashiwazaki S (1995) Expression and function of Fas antigen and bd-2 in human systemic lupus erythematosus lymphocytes. Clin Immunol Immunopath 73: 109–114
Mehrian R, Quismorio FP Jr, Strassmann G, Stimmler MM, Horwitz DA, Kitridou RC, Gauderman WJ, Morrison J, Brautbar C, Jacob CO (1998) Synergistic effect between IL-10 and bc1–2 genotypes in determining susceptibility to systemic lupus erythematosus. Arthritis Rheum 41: 596–602
Georgescu L, Vakkalanka RK, Elkon KB, Crow MK (1997) Interleukin-10 promotes activation-induced cell death of SLE lymphocytes mediated by Fas ligand. J Clin Invest 100: 2622–2633
Tsokos GC, Kovacs B, Liossis SN (1997) Lymphocytes, cytokines, inflammation, and immune trafficking. Curr Opin Rheumatol 9: 380–386
Yang BC, Wang YS, Lin LC, Liu MF (1997) Induction of apoptosis and cytokine gene expression in T-cell lines by sera of patients with systemic lupus erythematosus. Scand J Immunol 45: 96–102
Mysler E, Bini P, Drappa J, Ramos P, Friedman SM, Krammer PH, Elkon KB (1994) The apoptosis-1/Fas protein in human systemic lupus erythematosus. J Clin Invest 93: 1029–1034
Kovacs B, Tsokos GC (1995) Cross-linking of the Fas/APO-1 antigen suppresses the CD3-mediated signal transduction events in human T lymphocytes. J Immunol 155: 5543–5549
Nakajima M, Nakajima A, Kayagaki N, Honda M, Yagita H, Okumura K (1997) Expression of Fas ligand and its receptor in cutaneous lupus: implication in tissue injury. Clin Immun Immunopath 83: 223–229
Kovacs B, Liossis SN, Dennis GJ, Tsokos GC (1997) Increased expression of functional Fas-ligand in activated T cells from patients with systemic lupus erythematosus. Autoimmunity 25: 213–221
McNally J, Yoo DH, Drappa J, Chu JL, Yagita H, Friedman SM, Elkon KB, (1997) Fas ligand expression and function in systemic lupus erythematosus. J Immunol 159: 4628–4636
Feng Y (1997) Studies on Fas ligand expression in patients with systemic lupus erythematosus. Hokkaido Igaku Zasshi ¡ª Hokkaido J Med Science 72: 443–455
Kovacs B, Szentendrei T, Bednarek JM, Pierson MC, Mountz JD, Vogelgesang SA, Tsokos GC (1997) Persistent expression of a soluble form of Fas/APO1 in continuously activated T cells from a patient with SLE. Clin Exp Rheumatol 15: 19–23
Cheng J, Liu C, Koopman WJ, Mountz JD (1995) Characterization of human Fas gene. J Immunol 154: 1239–1245
Cheng J, Zhou T, Liu C, Shapiro JP, Brauer MJ, Kiefer MC, Barr PJ, Mountz JD (1994) Protection from Fas-mediated apoptosis by a soluble form of the Fas molecule. Science 263: 1759–1764
Liu C, Cheng J, Mountz JD (1995) Differential expression of human Fas mRNA species upon peripheral blood mononuclear cell activation. Biochem J 310: 957–963
Tokano Y, Miyake S, Kayagaki N, Nozawa K, Morimoto S, Azuma M, Yagita H, Takasaki Y, Okumura K, Hashimoto H (1996) Soluble Fas molecule in the serum of patients with systemic lupus erythematosus. J Clin Immunol 16: 261–265
Tokano Y. Miyake S. Kayagaki N. Nozawa K. Morimoto S. Azuma M. Yagita H. Takasaki Y. Okumura K. Hashimoto H (1996) Soluble Fas molecule in the serum of patients with systemic lupus erythematosus. J Clin Immunol 16: 261–265
Mountz JD, Zhou T, Cheng J (1996) Use of sensitive assays to detect soluble Fas in patients with systemic lupus erythematosus: comment on the article by Knipping, et al and the article by Goel, et al. Arthritis Rheum 39: 1611–1612
Okubo M, Ishida H, Kasukawa R (1996) Elevated levels of soluble Fas in systemic lupus erythematosus: comment in the article by Knipping et al. Arthritis Rheum 39: 1612–1614
Jodo S, Kobayashi S, Kayagaki N, Ogura N, Feng Y, Amasaki Y, Fujisaku A, Azuma M, Yagita H., Okumura K, Koike T (1997) Serum levels of soluble Fas/APO-1 (CD9S) and its molecular structure in patients with systemic lupus erythematosus (SLE) and other autoimmune diseases. Clin Exp Immunol 107: 89–95
Rose LM. Latchman DS. Isenberg DA (1997) Elevated soluble fas production in SLE correlates with HLA status not with disease activity. Lupus 6: 717–722
Nozawa K. Kayagaki N. Tokano Y. Yagita H. Okumura K. Hasimoto H (1997) Soluble Fas (APO-1, CD95) and soluble Fas ligand in rheumatic diseases. Arthritis Rheum 40: 1126–1129
Goel N, Ulrich DT, St. Clair EW, Fleming JA, Lynch DH, Seldin MF (1995) Lack of correlation between serum soluble Fas/APO-1 levels and autoimmune disease. Arthritis Rheum 38: 1738–1743
Knipping E, Krammer PH, Onel KB, Lehman TJ, Mysler E, Elkon KB (1995) Levels of soluble Fas/APO-1/CD95 in systemic lupus erythematosus and juvenile rheumatoid arthritis. Arthritis Rheum 38: 1735–1737
Tanaka M, Itai T, Adachi M, Nagata S (1998) Downregulation of Fas ligand by shedding. Nature Med 4: 31–36
Gilpin BJ, Loechel F, Mattei MG, Engvall E, Albrechtsen R, Wewer UM (1998) A novel, secreted form of human ADAM 12 (meltrin alpha) provokes myogenesis in vivo. J Biol Chem 273: 157–166
Kuno K, Kanada N, Nakashima E, Fujiki F, Ichimura F, Matsushima K (1997) Molecular cloning of a gene encoding a new type of metalloproteinase-disintegrin family protein with thrombospondin motifs as an inflammation associated gene. J Biol Chem 272: 556–562
Yoshiyama K, Higuchi Y, Kataoka M, Matsuura K, Yamamoto S (1997) CD156 (human ADAMS): expression, primary amino acid sequence, and gene location. Genomics 41: 56–62
Yuan R, Primakoff P, Myles DG (1997) A role for the disintegrin domain of cyritestin, a sperm surface protein belonging to the ADAM family, in mouse sperm-egg plasma membrane adhesion and fusion. J Cell Biol 137: 105–112
Rosendahl MS, Ko SC, Long DL, Brewer MT, Rosenzweig B, Hedl E, Anderson L, Pyle SM, Moreland J, Meyers MA, Kohno T, Lyons D, Lichenstein HS (1997) Identification and characterization of a pro-tumor necrosis factor-alpha-processing enzyme from the ADAM family of zinc metalloproteases. J Biol Chem 272: 24588–24593
Wu E, Croucher PI, McKie N (1997) Expression of members of the novel membrane linked metalloproteinase family ADAM in cells derived from a range of haematological malignancies. Biochem Biophys Res Commun 235: 437–442
Alderson MR, Tough TW, Davis-Smith T, Braddy S, Falk B, Schooley KA, Goodwin RG, Smith CA, Ramsdell F, Lynch DH (1995) Fas ligand mediates activation-induced cell death in human T lymphocytes. J Exp Med 181: 71–77
Dhein J, Walczak H, Baumler C, Debatin KM, Krammer PH (1995) Autocrine T-cell suicide mediated by APO-1/(Fas/CD95). Nature 373: 438–441
Brunner T, Mogil RJ, LaFace D, Yoo NJ, Manboubl A, Echeverre F, Martin J, Force WR, Lynch DH, Ware CF, Green DR (1995) Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T-cell hybridomas. Nature 373: 441–444
Kabelitz D, Pohl T, Pechhold K (1993) Activation-induced cell death (apoptosis) of mature peripheral T lymphocytes. Immunol Today 14: 338–339
Klas C, Debatin KM, Jonker RR, et al (1993) Activation interferes with the APO-1 pathway in mature human T cells. Intl Immunol 5: 625–630
Bossu P, Singer GG, Andres P, Ettinger R, Marshak-Rothstein A, Abbas AK (1993) Mature CD4+ T lymphocytes from MRL/Ipr mice are resistant to receptor-mediated tolerance and apoptosis. J Immunol 151: 7233–7239
Green DR, Scott DW (1994) Activation-induced apoptosis in lymphocytes. Curr Opin Immunol 6: 476–483
Tucek-Szabo CL, Andjelic S, Lacy E, Elkon KB, Nikolic-Zugic J (1996) Surface T cell Fas receptor/CD95 regulation, in vivo activation, and apoptosis. Activation-induced death can occur without Fas receptor. J Immunol 156: 192–200
Dhein J, Walczak H, Baumler C, Debatin KM, Krammer PH (1995) Autocrine T-cell suicide mediated by APO-1/(Fas/CD95). Nature 373: 438–441
Rathmell JC, Cooke MP, Ho WY, Grein J, Townsend SE, Davis MM, Goodnow CC (1995) CD95 (Fas)-dependent elimination of self-reactive B cells upon interaction with CD4’ T cells. Nature 376: 181–184
Scott DW, Grdina T, Shi Y (1996) T cells commit suicide, but B cells are murdered. J Immunol 156: 2352–2356
Cheng J, Liu C, Yang P, Zhou T, Mountz JD (1997) Increased lymphocyte apoptosis in Fas ligand transgenic mice. J Immunol 159: 674–684
Su X, Cheng J, Liu W, Liu C, Wang Z, Yang P, Zhou T, Mountz JD (1998) Autocrine and paracrine apoptosis are mediated by differential regulation of Fas ligand activity in two distinct Jurkat T cell populations. J Immunol 160: 5288–5293
Itoh N, Nagata S (1993) A novel protein domain required for apoptosis. Mutational analysis of human Fas antigen. J Biol Chem 268: 10932–10937
Tartaglia LA, Ayres TM, Wong GH, Goeddel DV (1993) A novel domain within the 55 kd TNF receptor signals cell death. Cell 74: 845–853
Kischkel FC, Hellbardt S, Behrmann I, Germer M, Pawlita M, Krammer PH, Peter ME (1995) Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor. EMBO J 14: 5579–5588
Chinnaiyan AM, O’Rourke K, Tewari M, Dixit VM (1995) FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis. Cell 81: 505–512
Cuvillier O, Rosenthal DS, Smulson ME, Spiegel S (1998) Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas-and ceramide-mediated apoptosis in Jurkat T lymphocytes. J Biol Chem 273: 2910–1916
Chinnaiyan AM, Tepper CG, Seldin MF, O’Rourke K, Kischkel FC, Hellbardt S, Kram-mer PH, Peter ME, Dixit VM (1996) FADD/MORT1 is a common mediator of CD95 (Fas/APO-1) and tumor necrosis factor receptor-induced apoptosis. J Biol Chem 271: 4961–4965
Varfolomeev EE, Boldin MP, Goncharov TM, Wallach D (1996) A potential mechanism of “cross-talk” between the p55 tumor necrosis factor receptor and Fas/APO1: proteins binding to the death domains of the two receptors also bind to each other. J Exp Med 183: 1271–1275
Kim PK, Dutra AS, Chandrasekharappa SC, Puck JM (1996) Genomic structure and mapping of human FADD, an intracellular mediator of lymphocyte apoptosis. J Immunol 157: 5461–5466
Hsu H, Xiong J, Goeddel DV (1995) The TNF receptor 1-associated protein TRADD signals cell death and NF-kappa B activation. Cell 81: 495–504
Hsu H, Shu HB, Pan MG, Goeddel DV (1996) TRADD-TRAF2 and TRADD-FADD interactions define two distinct TNF receptor 1 signal transduction pathways. Cell 84: 299–308
Boldin MP, Goncharov TM, Goltsev YV, Wallach D (1996) Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death. Cell 85: 803–815
Boldin MP, Varfolomeev EE, Pancer Z, Mett IL, Camoni JH, Wallach D (1995) A novel protein that interacts with the death domain of Fas/APO-1 contains a sequence motif related to the death domain. J Biol Chem 270: 7795–7798
Muzio M, Chinnaiyan AM, Kischkel FC, O’Rourke K, Shevchenko A, Ni J, Scaffidi C, Bretz JD, Zhang M, Gentz R, Mann M, Krammer PH, Peter ME, Dixit VM (1996) FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex. Cell 85: 817–827
Peter ME, Kischkel FC, Scheuerpflug CG, Medema JP, Debatin KM, Krammer PH (1997) Resistance of cultured peripheral T cells towards activation-induced cell death involves a lack of recruitment of FLICE (MACH/caspase 8) to the CD95 death-inducing signaling complex. Eur J Immunol 27: 1207–1212
Vincenz C, Dixit VM (1997) Fas-associated death domain protein interleukin-1betaconverting enzyme 2 (FLICE2), an ICE/Ced-3 homologue, is proximally involved in CD95- and p55-mediated death signaling. J Biol Chem 272: 6578–6583
Goltsev YV, Kovalenko AV, Arnold E, Varfolomeev EE, Brodianskii VM, Wallach D (1997) CASH, a novel caspase homologue with death effector domains. J Biol Chem 272: 19641–19644
Stanger BZ, Leder P, Lee TH, Kim E, Seed B (1995) RIP: a novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death. Cell 81: 513–523
Hsu H, Huang J, Shu HB, Baichwal V, Goeddel DV (1996) TNF-dependent recruitment of the protein kinase RIP to the TNF receptor-1 signaling complex. Immunity 4: 387–396
Grimm S, Stanger BZ, Leder P (1996) RIP and FADD: two “death domain”-containing proteins can induce apoptosis by convergent, but dissociable, pathways. Proc Natl Acad Sci USA 93: 10923–10927
Liu ZG, Hsu H, Goeddel DV, Karin M (1996) Dissection of TNF receptor 1 effector functions: JNK activation is not linked to apoptosis while NF-kappaB activation prevents cell death. Cell 87: 565–576
Ting AT, Pimentel-Muinos FX, Seed B (1996) RIP mediates tumor necrosis factor receptor 1 activation of NF-kappaB but not Fas/APO-1-initiated apoptosis. EMBO J 15: 6189–6196
Muzio M, Stockwell BR, Stennicke HR, Salvesen GS, Dixit VM (1998) An induced proximity model for caspase-8 activation. J Biol Chem 273: 2926–2930
Chou KC, Jones D, Heinrikson RL (1997) Prediction of the tertiary structure and substrate binding site of caspase-8. FEBS Letters 419: 49–54
Yang X, Khosravi-Far R, Chang HY, Baltimore D (1997) Daxx, a novel Fas-binding protein that activates JNK and apoptosis. Cell 89: 1067–1076
Duan H, Dixit VM (1997) RAIDD is a new `death’ adaptor molecule. Nature 385: 86–89
Sato T, Irie S, Reed JC (1995) A novel member of the TRAF family of putative signal transducing proteins binds to the cytosolic domain of CD40. FEBS Letters 358: 113–118
Rothe M, Xiong J, Shu HB, Williamson K, Goddard A, Goeddel DV (1996) I-TRAF is a novel TRAF-interacting protein that regulates TRAF-mediated signal transduction. Proc Natl Acad Sci USA 93: 8241–8246
Natoli G, Costanzo A, Ianni A, Templeton DJ, Woodgett JR, Balsano C, Levrero M (1997) Activation of SAPK/JNK by TNF receptor 1 through a noncytotoxic TRAF2dependent pathway. Science 275: 200–203
Ishida TK, Tojo T, Aoki T, Kobayashi N, Ohishi T, Watanabe T, Yamamoto T, Inoue J (1996) TRAF5, a novel tumor necrosis factor receptor-associated factor family protein, mediates CD40 signaling. Proc Natl Acad Sci USA 93: 9437–9442
Cao Z, Xiong J, Takeuchi M, Kurama T, Goeddel DV (1996) TRAF6 is a signal transducer for interleukin-1. Nature 383: 443–446
Rothe M, Pan MG, Henzel WJ, Ayres TM, Goeddel DV (1995) The TNFR2-TRAF signaling complex contains two novel proteins related to baculoviral inhibitor of apoptosis proteins. Cell 83: 1243–1252
Beg AA, Baldwin AS (1996) An essential role for NF-KB in preventing TNFŒ-induced cell death. Science 274, 782–784
Rothe M, Sarma V, Dixit VM, Goeddel DV (1995) TRAF2-mediated activation of NFkB by TNF receptor 2 and CD40. Science 269: 1424–1427
Song HY, Rothe M, Goeddel DV (1996) The tumor necrosis factor-inducible zinc finger protein A20 interacts with TRAF1/TRAF2 and inhibits NF-kappaB activation. Proc Natl Acad Sci USA 93: 6721–6725
Takeuchi M, Rothe M, Goeddel DV (1996) Anatomy of TRAF2 Distinct domains for nuclear factor-kappaB activation and association with tumor necrosis factor signaling proteins. J Biol Chem 271: 19935–19942
Malinin NL, Boldin MP, Kovalenko AV, Wallach D (1997) MAP3K-related kinase involved in NF-kappaB induction by TNF, CD95 and IL-1. Nature 385: 540–544
Wesche H, Henzel WJ, Shillinglaw W, Li S, Cao Z (1997) MyD88: an adapter that recruits IRAK to the IL-1 receptor complex. Immunity 7: 837–847
Regnier CH, Tomasetto C, Moog-Lutz C, Chenard MP, Wendling C, Basset P, Rio MC (1995) Presence of a new conserved domain in CART1, a novel member of the tumor necrosis factor receptor-associated protein family, which is expressed in breast carcinoma. J Biol Chem 270: 25715–25721
Pan G, O’Rourke K, Chinnaiyan AM, Gentz R, Ebner R. Ni J, Dixit VM (1997) The receptor for the cytotoxic ligand TRAIL. Science 276: 111–113
Pan G, Ni J, Wei YF, Yu G, Gentz R, Dixit VM (1997) An antagonist decoy receptor and a death domain-containing receptor for TRAIL. Science 277: 815–818
Kitson J, Raven T, Jiang YP, Goeddel DV, Giles KM, Pun KT, Grinham CJ, Brown R, Farrow SN (1996) A death-domain-containing receptor that mediates apoptosis. Nature 384: 372–375
Chinnaiyan AM, O’Rourke K, Yu GL, Lyons RH, Garg M, Duan DR, Xing L, Gentz R, Ni J, Dixit VM (1996) Signal transduction by DR3, a death domain-containing receptor related to TNFR-1 and CD95. Science 274: 990–992
Chaudhary PM, Eby M, Jasmin A, Bookwalter A, Murray J, Hood L (1997) Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-KB pathway. Immunity 7: 821–830
Schneider P, Thome M, Burns K, Bodmer JL, Hofmann K, Kataoka T, Holler N, Tschopp J,(1997) TRAIL receptors 1 (DR4) and 2 (DR5) signal FADD-dependent apoptosis and activate NF-KB. Immunity 7: 831–836
Wong BR, Rho J, Arron J, Robinson E, Orlinick J, Chao M, Kalachikov S, Cayani E, Bartlett FS 3rd, Frankel WN, Lee SY, Choi Y (1997) TRANCE is a novel ligand of the tumor necrosis factor receptor family that activates c-Jun N-terminal kinase in T cells. J Biol Chem 272: 25190–25194
Aragane Y, Kulms D, Metze D, Wilkes G, Poppelmann B, Luger TA, Schwarz T (1998) Ultraviolet light induces apoptosis via direct activation of CD95 (Fas/APO-1) independently of its ligand CD95L. J Cell Biol 140: 171–182
Malinin NL, Boldin MP, Kovalenko AV, Wallach D (1997) MAP3K-related kinase involved in NF-kappaB induction by TNF, CD95 and IL-1. Nature 385: 540–544
Rehemtulla A, Hamilton CA, Chinnaiyan AM, Dixit VM (1997) Ultraviolet radiation-induced apoptosis is mediated by activation of CD-95 (Fas/APO-1). J Biol Chem 272: 25783–25786
Burmester GR, Daser A, Kamradt T, Krause A, Mitchison NA, Sieper J, Wolf N (1995) Immunology of reactive arthritides. Annu Rev Immunol 13: 229–250
Braun J, Laitko S, Treharne J, Eggens U, Wu P, Distler A, Sieper J (1994) Chlamydia pneumoniae-a new causative agent of reactive arthritis and undifferentiated oligoarthritis. Ann Rheum Dis 53: 100–105
Taylor-Robinson D, Gilroy CB, Thomas BJ, Keat ACS (1992) Detection of chlamydia trachomatis DNA in joints of reactive arthritis patients by polymerase chain reaction. Lancet 340: 81–82
Heusel JW, Wesselschmidt RL, Shresta S, Russell JH, Ley TJ (1994) Cytotoxic lymphocytes require granzyme B for the rapid induction of DNA fragmentation and apoptosis in allogeneic target cells. Cell 76: 977–987
Rahman MU, Cheema MA, Schumacher HR, Hudson AR.(1992) Molecular evidence for the presence of chlamydia in the synovium of patients with Reiter’s syndrome. Arthritis Rheum 35: 521–529
Holland SM, Hudson AP, Bobo L, Whittum-Hudso JA et al (1992) Demonstration of chlamydial RNA and DNA during a culture-negative state. Infect Immun 60: 2040–2047
Schmita E, Nettelnbreker E, Zeidler H, Hammer M, Manor E, Wollenhaupt J (1993) Intracellular persistence of chlamydial major outermembrane protein, lipopolysaccharide and ribosomal RNA after non-productive infection of human monocytes with Chlamydia trachomatis serovar K. J Med Microbiol 38: 278–285
Ornstein MH, Kerr LD, Spiera H (1995) A reexamination of the relationship between active rheumatoid arthritis and the acquired immunodeficiency syndrome. Arthritis Rheum 38: 1701–1706
Muller-Ladner U, Kriegsmann J, Gay RE, Koopman WJ, Gay S, Chatham WW (1995) Progressive joint destruction in a human immunodeficiency virus-infected patient with rheumatoid arthritis. Arthritis Rheum 38: 1328–1332
Iwakura Y, Saijo S, Kioka Y, Nakayama-Yamada J, et al.(1995) Autoimmunity induction by human T cell leukemia virus type 1 in transgenic mice that develop chronic inflammatory arthropathy resembling rheumatoid arthritis in humans. J Immunol 155: 1588–1598
Ferraccioli GF, Casatta L, Bartoli E, De Vita S et al (1995) Epstein-Barr virus-associated Hodgkin’s lymphoma in a rheumatoid arthritis patient treated with methotrexate and cyclosporin A. Arthritis Rheum 38: 867–868
Westendorp MO, Frank R, Ochsenbauer C, Stricker K et al (1995) Sensitization of T cells to CD95-mediated apoptosis by HIV-1 Tat and gp120. Nature 375: 497–500
Katsikis PD, Wunderlich ES, Smith CA, Herzenberg LA, Herzenberg LA (1995) Fas antigen stimulation induces marked apoptosis of T lymphocytes in human immunodeficiency virusinfected individuals. J Exp Med 181: 2029–2036
Takizawa T, Fukuda R, Miyawaki T, Ohashi K, Nakanishi Y (1995) Activation of the apoptotic Fas antigen-encoding gene upon influenza virus infection involving spontaneously produced beta-interferon. Virol 209: 288–296
Darmon AJ, Nicholson DW, Bleackley RC (1995) Activation of the apoptotic protease CPP32 by cytotoxic T-cell-derived granzyme B. Nature 377: 446–448
Geiger KD, Gurushanthaiah D, Howes EL, Lewandowski GA et al (1995) Cytokine-mediated survival from lethal herpes simplex virus infection: role of programmed neuronal death. Proc Natl Acad Sci USA 92: 3411–3415
Tarodi B, Subramanian T, Chinnadurai G (1994) Epstein-Barr virus BHRF1 protein protects against cell death induced by DNA-damaging agents and heterologous viral infection. Virol 201: 404–407
Thome M, Schneider P, Hofmann K, Fickenscher H, Meinl E, Neipel F, Mattmann C, Burns K, Bodmer JL, Schroter M, Scaffidi C, Krammer PH, Peter ME, Tschopp J (1997) Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptors. Nature 386: 517–521
Izumi KM, Kieff ED (1997) The Epstein-Barr virus oncogene product latent membrane protein 1 engages the tumor necrosis factor receptor-associated death domain protein to mediate B lymphocyte growth transformation and activate NF-KB. Proc Natl Acad Sci USA 94: 12592–12597
Hu S, Vincenz C, Ni J, Gentz R, Dixit VM (1997) I-FLICE, a novel inhibitor of tumor necrosis factor receptor-1- and CD-95-induced apoptosis. J Biol Chem 272: 17255–17257
Irmler M, Thome M, Hahne M, Schneider P, Hofmann K, Steiner V, Bodmer JL, Schrot-er M, Burns K, Mattmann C, Rimoldi D, French LE, Tschopp J (1997) Inhibition of death receptor signals by cellular FLIP. Nature 388: 190–195
Thome M, Schneider P, Hofmann K, Fickenscher H, Meinl E, Neipel F, Mattmann C, Burns K, Bodmer JL, Schroter M, Scaffidi C, Krammer PH, Peter ME, Tschopp J (1997) Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptors. Nature 386: 517–521
Daniels T, Talai N (1987) Diagnosis and differential diagnosis of Sjögren’s Syndrome. In: Talai N, Moutsopoulos HM, Kassan SS (eds): Sjögren’s Syndrome: clinical and immunological aspects. Springer-Verlag, Berlin
Fox RI, Maruyama T (1997) Pathogenesis and treatment of Sjögren’s Syndrome. Curr Opin Rheumatol 9: 393–399
Fox RI (1996) Clinical features, pathogenesis, and treatment of Sjögren’s Syndrome. Curr Opin Rheumatol 8: 438–445
Talal N, Dang H (1997) Fas and Fas ligand expression in the salivary glands of patients with primary Sjögren’s Syndrome. Arthritis Rheum 40: 87–97
Sumida T, Matsumoto I, Murata H, Namekawa T, Matsumura R, Tomoika H, Iwamoto I, Saito Y, Mizushima Y, Hasunuma T, Maeda T, Nishioka K (1997) TCR in Fas-sensitive T cells from labial salivary glands of patients with Sjögren’s Syndrome. J Immunol 158: 1020–1025
Ichikawa Y, Arimori K, Yoshida M, Horiki T, Morita K, Uchiyama M, Shimizu H, Moriuchi J, Takaya M (1995) Abnormal expression of apoptosis-related antigens, Fas and bd-2, on circulating T lymphocyte subsets in primary Sjögren’s Syndrome. Clin Exp Rheumatol 13: 307–313
Koike K, Moryia K, Ishibashi K, Yotsuyanagi H, Shintani Y, Fujie H, Kurokawa K, Matsuura Y, Miyamura T (1997) Sialadenitis histologically resembling Sjögren’s Syndrome in mice transgenic for hepatitis C virus envelope genes. Proc Natl Acad Sci USA 94: 233–236
Scott CA, Avellini C, Desinan L, Pirisi M, Ferraccioli GF, Bardus P, Fabris C, Casatta L, Bartoli E, Beltrami CA (1997) Chronic lymphocytic sialadenitis in HCV-related chronic liver disease: comparison of Sjögren’s Syndrome. Histopathology 30: 41–48
Haddad J, Deny P, Munz-Gotheil C, Ambrosini JC, Trinchet JC, Pateron D, Mal F, Callard P, Beaugrand M (1992) Lymphocytic sialadenitis of Sjögren’s Syndrome associated with chronic hepatitis C virus liver disease. Lancet 339: 321–323
Wen S, Shimizu N, Yoshiyama H, Mizugaki Y, Shinozaki F, Takada K (1996) Association of Epstein-Barr virus (EBV) with Sjögren’s Syndrome: differential EBV expression patterns between epithelial cells and lymphocytes in salivary glands. Am J Pathol 149: 1511–1517
Maitland N, Flint S, Scully C, Crean SJ (1995) Detection of cytomegalovirus and Epstein-Barr virus in labial salivary glands in Sjögren’s Syndrome and non-specific sialadenitis. J Oral Pathol Med 24: 293–298
Syrjanen S, Karja V, Chang FJ, Johansson B, Syrjanen K (1990) Epstein-Barr virus involvement in salivary gland lesions associated with Sjögren’s Syndrome. ORL J Otorhinolaryngol Relat Spec 52: 254–259
Clark DA, Lamey PJ, Jarett RF, Onions DE (1994) A model to study viral and cytokine involvement in Sjögren’s Syndrome. Autoimmunity 18: 7–14
Wittingham S, McNeilage J, Mackay IR (1985) Primary Sjögren’s Syndrome after mononucleosis. Ann Intern Med 102: 490–493
Newkirk MM, Shiroky JB, Johnson N, Danoff D, Isenberg DA, Shustik C, Pearson GR (1996) Rheumatic disease patients, prone to Sjögren’s Syndrome and/or lymphoma, mount an antibody response to BHRF1, the Epstein-Barr viral homologue of BCL-2. Br J Rheumatol 35: 1075–1081
Thorn JJ, Oxholm P, Andersen HK (1988) High levels of complement fixing antibodies against cytomegalovirus in patients with primary Sjögren’s Syndrome. Clin Exp Rheumatol 6: 71–74
Wax TD, Layfield LJ, Zaleski S, Bhargara V, Cohen M, Lyerly HK, Fisher SR (1994) Cytomegalovirus sialadenitis in patients with the acquired immunodeficiency syndrome: a potential diagnostic pitfall with fine-needle aspiration cytology. Diagn Cytopathol 10: 169–172
Schiodt M, Greenspan D, Daniels TE, Nelson J, Legott PJ, Wara DW, Greenspan JS (1989) Parotid gland enlargement and xerostomia associated with labial sialadenitis in HIV-infected patients. J Autoimmun 2: 415–425
Britt WJ, Alford CA (1996) In: Fields BN, Knipe DM, Howley PM (eds): Fields virology. Lippinscott-Raven, Philadelphia, PA
Messerle M, Keil GM, Schneider K, Koszinowski UH (1992) Characterization of the murine cytomegalovirus genes encoding the major DNA binding protein and the ICP18 5 homolog. Virology 191: 355–367
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1999 Springer Basel AG
About this chapter
Cite this chapter
Song, G.G., Fleck, M., Wu, J., Hsu, HC., Zhou, T., Mountz, J.D. (1999). Lupus and lupus-like syndromes. In: Winkler, J.D. (eds) Apoptosis and Inflammation. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8741-0_11
Download citation
DOI: https://doi.org/10.1007/978-3-0348-8741-0_11
Publisher Name: Birkhäuser, Basel
Print ISBN: 978-3-0348-9752-5
Online ISBN: 978-3-0348-8741-0
eBook Packages: Springer Book Archive