Cytokines in autoimmunity

Current Opinion in Immunology

Volumn 8, Issue 6, 1996, Pages 872-877

  Brennan, Fionula M ^a   Feldmannt, Marc ^a  

^a UNIVERSITY OF OXFORD   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE; TUMOR NECROSIS FACTOR ALPHA ANTIBODY;

AUTOIMMUNITY; CROHN DISEASE; DRUG THERAPY; ETIOLOGY; RHEUMATOID ARTHRITIS; SHORT SURVEY;

EID: 0030457664     PISSN: 09527915     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0952-7915(96)80018-5     Document Type: Article

References (63)

1. Brennan FM, Feldmann MF. Cytokines in Autotmmunity. Austin, Texas: RC Landes Company; 1996.
2. Feldmann M, Brennan FM, Maini RN: Role of cytokines in rheumatoid arthritis. Annu Rev Immunol 1996, 14:397-440.
3. Butler DM, Maini RN, Feldmann M, Brennan FM: Modulation of proinflammatory cytokine release in rheumatoid synovial membrane cell cultures. Comparison of monoclonal anti-TNFa antibody with the IL-1 receptor antagonist Eur Cytokine Network 1995, 6:225-230.
4. Proben L, Plows D, Kontogeorgos G, Kollias G: The type 1 interleukin-1 receptor acts in series with tumor necrosis factor (TNF) to induce arthritis in TNF- transgenic mice. Fur J Immunol 1995, 25:1794-1 797.
5. Elliolt MJ, Maini RN, Feldmann M, Kalden JR, Amoni C, Smolen JS, Leeb B, Breedveld FC, Macfarlane JD, Bijl H et al.: Randomised double blind comparison of a chimaeric monoclonal antibody to tumour necrosis factor a (cA2) versus placebo in rheumatoid arthritis. Lancet 1994, 344:1105-1110.
6. Elliott MJ, Maini RN, Feldmann M, Long-Fox A, Charles P, Bijl H, Woody JN: Repeated therapy with monoclonal antibody to tumour necrosis factor ot (cA2) in patients with rheumatoid arthritis. Lancet 1994, 344:1125-1127.
7. Rankin ECC, Choy EHS, Kassitnos D, Kingsley GH, Sopwith SM, Isenberg DA, Panayi GS: The therapeutic effects of an engineered human anti-tumour necrosis factor alpha antibody (CDP571) in rheumatoid arthritis. Br i Rheumatol 1995, 34:334-342. This paper describes a double-blind trial in which the humanized TNF antibody CDP571 administered intravenously in single doses of 0.1, 1.0 or 10mgkg-1 to patients with active RA (n=24), was compared with placebo (n=12). CDP571 at the higher dose (lOmgkg-1) caused a significant reduction in erythrocyte sedimentation rate, C reactive protein and the number of tender joints, maximally after one or two weeks.
8. Moreland LW, Margolies GR, Heck LW, Saway PA, Jacobs C, Beck C, Blosch C, Koopman WJ: Soluble tumor necrosis factor receptor (sTNFR):- results of a phase I dose-escalation study in patients with rheumatoid arthritis [abstract]. Arthritis Rheum 1994, 32(suppl):295.
9. -1). In parallel, a rapid and sustained increase in circulating lymphocyte counts was observed, with largest changes observed in patients in whom a. clinical benefit (≥20% Paulus response at week four) was observed.
10. Tak PP, Taylor PC, Breedveld FC, Smeets TJM, Kluin PM, Meinders AE, Maini RN: Decrease in cellularity and expression of adhesion molecules by anti-tumor necrosis factor a monoclonal antibody treatment in patients with rheumatoid arthritis. Arthritis Rheum 1996, 39: 1092-1101.
11. Cope AP, Londei M, Chu NR, Cohen SBA. Elliott MJ, Maini RN, Brennan FM, Feldmann M: Chronic exposure to tumor necrosis factor (TNF) in vitro impairs the activation of T cells through the T cell receptor/CD3 complex; reversal in vivo by anti-TNF antibodies In patients with rheumatoid arthritis. J Clin Invest 1994, 94:749-760.
12. Lai NS, Lan JL, Yu CL, Lin RH: Role of tumor necrosis factoralpha in the regulation of activated synovial T cell growth: down-regulation of synovial T cells in rheumatoid arthritis patients. Eur J Immunol 1995, 25:3243-3248.
13. Maini RN, Elliott MJ, Brennan FM, Williams RO, Chu CQ, Paieolog E, Charles PJ, Taylor PC, Feldmann M: Monoclonal anti-TNF antibody as a probe of pathogenesis and therapy of rheumatoid disease. Immunol Rev 1995, 144:195-223.
14. Van Dullemen HM, Van Deventar SJH, Hommes DW, Bijl HA, Jan sen J, Tytgat GNJ, Woody J: Treatment of Crohn's disease with anti-tumor necrosis factor chimeric monoclonal antibody (cA2). Gastroenterology 1995, 109:129-135. This paper describes for the first time the efficacy of cA2 therapy m an openlabel treatment protocol of ten patients with active Crohn's disease who were previously unresponsive to steroid treatment. Eight patients showed normalization of Crohn's disease activity index scores and healing of ulcerations as judged by colonoscopy within four weeks of treatment with a single infusion of cA2, with an average duration of response of four months.
15. Raine CS: Multiple sclerosis: TNF revisited, with promise [comment]. Nat Med 1995, 1:211-214.
16. Probert L, Akassoglou K, Pasparakis M, Kontogeorgos G, Kollias G: Spontaneous inflammatory demyelinating disease in transgenic mice showing central nervous system-specific expression of tumor necrosis factor alpha Proc Natl Acad Sci USA 1995,92:11294-11298. This interesting study describes the spontaneous development of a chronic inflammatory demyelinating disease in transgenic mice that constitutively express a dysregulated murine TNF transgene under the control of its own promoter. Transgene expression was restricted to the CNS, with high-level expression in neurons distributed throughout the brain. The direct involvemenl of TNF in the pathogenesis of this disease was confirmed by peripheral administration of neutralizing murine mTNFa antibodies.
17. Sommer N, Loschmann P-A, Northoff GH, Weller M, Steinbrecher A. Steinbach JP, Lichtenfels R, Meyermann R, Riethmuller A, Fontana A et al.: The antidepressant rolipram suppresses cytokine production and prevents autoimmune encephalomyelitis. Nat Med 1995, 1:244-248.
18. Genain CP, Roberts T, Davis RL, Nguyen M-H, Uccelli A, Faulds D Li Y, Hedgpeth J. Hauser SL: Prevention of autoimmune demyelination in non-human primates by a cAMP-specific phosphodiesterase inhibitor. Proc Natl Acad Sci USA 1905, 92:3601-3605.
19. Maksymowych WP, Avina-Zubieta A, Luong MH, Russell AS: An open study of pentoxifylline in the treatment of severe refractory rheumatoid arthritis. J Rheumatol 1995, 22:625-829.
20. McGeehan GM, Becherer JD, Bast Jr RC, Boyer CM, Champion B, Connolly KM, Conway JG, Furdon P, Karp S, Kidao S et al.: Regulation of tumour necrosis factor a processing by a metalloproteinase inhibitor. Nature 1994, 370:558-561.
21. Mohler K, Sleath PR, Fitzner JN, Cerralti DP, Alderson M, Kerwar SS, Torrance DS, Otten-Evans C, Gresnstreet T, Weerawama K et al,: Protection against a lethal dose of endotoxin by an inhibitor of tumour necrosis factor processing. Nature 1994, 370:218-220.
22. Gearing AJH, Beckell P, Ctiristodoulou M, Churchill M, Clements J, Davidson AH, Drummond AH, Galloway WA, Gilbert R, Gordon JL et al.: Processing of tumour necrosis faclor-α precursor by metallaproteinases. Nature 1994, 370:555-557.
23. Crowe PD, Walter BN, Mohler KM, Otten-Evans C, Black RA, Ware CF: A metalloprotease inhibitor blocks shedding of the 80 kD TNF receptor and TNF processing in T lymphocytes. J Exp Med 1994, 181:1205-1210.
24. Williams L, Gibbons DL, Gearing A, Feldmann M, Brennan FM: Paradoxical effects of a synthetic metalloproteinase inhibitor which blocks both p55 and p75 TNF receptor shedding and TNFct processing. J Clin Invest 1996, 97:2833-2641. The results described in this paper raise the interesting possibility that a close relationship exists between the enzyme(s) which process membranebound TNFα, and those involved in surface TNF-R cleavage, and suggest that hydroxamate inhibitors of MMP activity which block TNFα secretion and TNF-R cleavage may not modulate downstream effects of TNFα. The precisa specificity of these compounds, therefore, will be highly relevant to their clinical efficacy in inflammatory diseases.
25. Brennan FM, Gibbons DL, Cope AR Katsikis P, Maini RN, Feldmann M: TNF inhibitors are produced spontaneously by rheumatoid and osteoarthritic synovial joint cell cultures: evidence of feedback control of TNF action. Scand J Immunol 1995, 42:158-165.
26. Georgopoulos S, Plows D, Kollias G: Transmembrane TNF is sufficient to induce localized tissue toxicity and chronic inflammatory arthritis in transgenic mice. J Inflamm 1996, 46:86-97.
27. Campion GV, Lebsack ME, Lookabaugh J, Gordon G, Catalano M, The IL-1 ra Arthritis Study Group: Dose-range and dose frequency study of recombinant human interleukin-1 receptor antagonist in patients with rheumatoid arthritis. Arthritis Rheum 1996, 39:1092-1101.
28. Drevlaw BE, Lovis R, Haag MA, Sinacora JM, Jacobs C, Blosche C, Landay A, Mcreland LW, Pape RM: Recombinant human interleukin-1 receptor type I in the treatment of patients with active rheumatoid arthritis. Arthritis Rheum 1998, 39:257-265.
29. Joasten LAB, Helsen MMA, Vandeloo FAJ, Vandenberg WB: Anticytokine treatment of established type II collagen-induced arthritis in DBA/1 mice: a comparative study using anti-TNF alpha, anti-IL-1 alpha/beta, and IL-1Ra. Arthritis Rheum 1996, 39:797-809.
30. Ku G, Faust T, Latffer LL, Livingston DJ, Harding MW: Interleukin-I beta converting enzyme inhibition blocks progression of type II collagen-induced arthritis in mice. Cytokire 1996, 8:377-386.
31. Firestein GS, Boyle DL, Yu C, Paine MM, Whisenand TO, Zvaifler NJ. Arend WP: Synovial interleukin-1 receptor antagonist and interleukin-1 balance in rheumatoid arthritis. Arthritis Rheum 1994,37:644-652.
32. Llorente L, Richaud-Patin Y, Fior R, Alcocer-Varela J, Wijdenes J, Fourrier B, Galanaud P, Emilie D: In vivo production of interleukin-10 by non-T cells in rheumatoid arthritis, Sjogren's syndrome, and systemic lupus erythematosus. Arthritis Rheum 1994, 37:1647-1655.
33. Katsikis P, Chu CO, Brennan FM, Maini RN, Feldmann M: Immunoregulatory role of interleukin 10 (IL-10) in rheumatoid arthritis. J Exp Wed 1994, 179:1517-1527.
34. Cush JJ, Splawski JB, Thomas R, McFarlin JE, Schulze-Koops H, Davis LS, Fujita K, Lipsky PE: Elevated interleukin-10 levels in patients with rheumatoid arthritis. Arthritis Rheum 1995, 38:96-104.
35. Chomarat P, Banchereau J, Miossec P: Differential effects of interieukins 10 and 4 on the production of interleukin-6 by blood and synovium monocytes in rheumatoid arthritis. Arthritis Rheum 1995, 38:1046-54.
36. Vanroon JAG, Vanroy J, Gmeligmeyling FHJ, Lafeber F, Bijlsma JWJ : Prevention and reversal of cartilage degradation in rheumatoid arthritis by interleukin-10 and interleukin-4. Arthritis Rheum 1996, 39:829-835.
37. Perez L, Orte J, Brieva JA: Terminal differentiation of spontaneous rheumatoid factor-secreting B cells from rheumatoid arthritis patients depends on endogenous interleukin-10. Arthritis Rheum 1995, 38:1771-1776.
38. Kasama T, Strieter RM, Lukacs NW, Lincoln PM, Burdick MD, Kunkel SL: Interleukin-10 expression and chemokine regulation during the evolution of murine type II collagen-induced arthritis. J Clin Invest 1995, 95:2868-2876. This interesting study demonstrates for the first time expression of chernokines during the evolution of CIA, the onset of which was delayed if administered with antibodies directed against either MIP-1 α or MIP-2. On the contrary, CIA mica receiving neutralizing IL-10 antibodies demonstrated an acceleration of the onset and an increase in the severity of arthritis.
39. Walmslay M, Katsikis PD, Abney E, Parry S, Williams RU, Maini RN, Feldmann M: Interleukin-10 inhibition of the progression of established collagen-induced arthritis. Arthritis Rheum 1996, 39:495-503.
40. Crisi GM, Santambrogio L, Hochwald GM, Smith SR, Carlino JA, Thorbecke GJ: Staphylococcal enterotoxin B and tumornecrosis factor-alpha-induced relapses of experimental allergic encephalomyelitis: protection by transforming growth factorbeta and interleukin-10. Eur J Immunol 1995, 25:3035-3040. This paper describes the ability of Staphylococcal enterotoxin B or INF to induce relapses of EAE in SJL mice. Administration of IL-10 and TGF-02 reduced these relapses, whilst anti-IL-10 increased both the incidence and the severity. The authors conclude that TNF production is probably important in causing EAE relapses, and that endogenous IL-10 rather than TGF-β production appears to limit the susceptibility to relapses in this model.
41. Mignon-Godefroy K, Rott O, Brazillet MP, Charreire J: Curative and protective effects of IL-10 in experimental autoimmune thyroiditis (EAT). Evidence for IL-10-enhanced cell death in EAT. J Immunol 1995, 154:6634-6643. This paper examines the effect of recombinant human IL-10 administration in two models of experimental autoimmune thyroiditis. Administration results in a significant reduction in seventy of disease but no change in level of anti-mTg (mouse thyroglobulin) autoantibody levels. Activation-induced cell death of autoreactive T lymphocytes was increased.
42. Kuhn R, Lohler J, Rennick O, Rajewsky K, Muller W: Interleukin-10-def)cient mice develop chronic enterocolitis. Cell 1993, 75:263-274.
43. Hagiwara E, Gourley MF, Lee S, Klinman DM: Disease severity in patients with systemic lupus erythematosus correlates with an increased ratio of interleukin-10: interferon-gammasecreting cells in the peripheral blood. Arthritis Rheum 1996, 39:379-385.
44. Ishida H, Muchamuel T, Sakagtchi S, Andrade S, Menon S, Howard M: Continuous administration of anti-interleukin 10 antibodies delays onset of autoimmunity in NZB/W F1 mice. J Exp Med 1994, 179:305-310.
45. Wogensen L, Huang X, Sarvetnick N: Leukocyte extravasation into the pancreatic tissue in transgenic mice expressing interleukin 10 in the islets of Langerhans. J Exp Med 1993, 178:175-185.
46. Wogensen L, Myung-Shik L, Sarvetnick N: Production of interleukin-10 by islet cells accelerates immune-mediated destruction of β cells in nonobese diabetic mice. J Exp Med 1994, 179:1379-1384.
47. Nicoletti F, Patti F, Dimarco R, Zaccone P, Niooletti A, Meroni PL, Reggio A: Circulating serum levels of IL-1ra in patients with relapsing remitting multiple sclerosis are normal during remission phases but significantly increased either during exacerbations or in response to IFN-beta treatment Cytokine 1996,8:395-400.
48. Porrini AM, Gambi D, Reder AT: Interferon effects on interleukin10 secretion. Mononuclear cell response to interleukin-10 is normal in multiple sclerosis patients. J Neuroimmunol 1995, 61:27-34.
49. Strieter RM, Standiford TJ, Huffnagle GB, Colletti LM, Lukacs NW, Kunkel SL: The good, the bad, and the ugly": the role of chemokines in models of human disease - commentary. J Immunol 1996, 156:3583-3586.
50. Kunkel SL, Lukacs N, Kasama T, Strieter RM: The role of chemokines in inflammatory joint disease. J Leukocyte Biol 1996, 59:6-12. A well written review describing the association of chemokines with RA, and information from animal models regarding the kinetics of production and contribution of specific mediators to the development of experimental arthritis.
51. Berman JW, Guida MR Warren J, Amat J, Brosnan CF: Localization of monocyte chemoattractant peptide-1 expression in the central nervous system in experimental autoimmune encephalomyelitis and trauma in the rat J Immunol 1996, 156:3017-3023.
52. Karpus WJ, Lukacs NW, McRae BU, Strieter RM, Kunkel SL, Miller SO: An important role for the chemokine macrophage inflammatory protein-1 alpha In the pathogenesis of the T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis. J Immunol 1995, 155:5003-5010.
53. 2b, antibodies.
54. Hess H, Gately MK, Rude E, Schmilt E, Szeliga J, Germann T: High doses of lnterleukin-12 inhibit the development of joint disease in DBA/1 mice immunized with type II collagen in complete Freund's adjuvant Cur J Immunol 1996, 26:197-191.
55. Lament AG, Adorin L: IL-12: a key cytokine in immune regulation. Immunoi Today 1996, 17:214-21 7.
56. Leonard JP, Waldburger KE, Goldman SJ: Prevention of experimental autoimmune encephalomyelitis by antibodies against interleukin 12. J Exp Med 1995, 181:381-386.
57. Neurath MF, Fuss I, Kelsall BL, Stuber E, Strober W: Antibodies to interleukin 12 abrogate established experimental colitis In mice. J Exp Med 1995, 182:1281-1290.
58. Trembleau S, Germann T, Gately MK, Adorini L: The role of IL-12 in the induction of organ-specific autoimmune diseases. Immunol Today 1995, 16:383-388. This review examines the role of IL-12, a key cytokine guiding the development of Th1 cells, in the induction of autoimmune diseases, and discusses potential immunointervention strategies based on administration of IL-12 antagonists.
59. Zipris D, Greiner DL, Malkani S, Whalen B, Mordes JP, Rossini AA: Cytokine gene expression in islets and thyroids of BB rats -IFN-gamma and IL-12p40 mfiNA increase with age in both diabetic and insulin-treated nondiabetic BB rats. J Immunol 1996, 156:1315-1321.
60. Rothe H, Burkart V, Faust A, Kolb H: Interleukin-12 gene expression is associated with rapid development of diabetes mellitus in non-obese diabetic mice. Diabetologia 1996, 39:119-122.
61. Windhagen A, Newcombe J, Dangond F, Strand C, Woodroofe MM, Cuzner ML, Hafler DA: Expression of costimulatory molecules B7-1 (CD30), B7-2 (CD86), and interleukin 12 cytokine in multiple sclerosis lesions. J Exp Med 1995, 182:1985-1996. This interesting paper describes increased expression of B7-1 and IL-12 p40 in acute MS plaques, particularly from early disease cases, but not in inflammatory infarcts, and speculates that an early event in the initiation of MS involves upregulation of B7-1 and IL-12, and results in conditions that maximally stimulate T cell activation and induction of Th1-type immune responses.
62. Magram J, Connaughton SE, Warrier RR, Carvajal DM, Wu C, Ferrante J, Stewart C, Sarmiento U, Faherty DA, Gately MK: It-12 deficient mice are defective in IFNy production and type 1 cytokine responses. Immunity 1996, 4:471-481.
63. Ferber IA, Brocke S, Taylor-Edwards C, Ridgway W, Dinisco C, Steinman L. Gallon D, Fathman CG: Mice with a disrupted IFNgamma gene are susceptible to the induction of experimental autoimmune encephalolmyelitis (EAE). J Immunol 1996, 156:5-7. This short report makes the interesting but unexpected finding that IFNy is not crucial for the induction or perpetuation of EAE. This is based on their observation that mice homozygous for deletion in the IFNy gene, back-crossed onto an EAE-susceptible strain, develop disease following immunization with MBP, with massive mononuclear cell infiltrates in the CMS.