Biologic agents in the treatment of inflammatory rheumatic diseases

Current Opinion in Rheumatology

Volumn 11, Issue 3, 1999, Pages 179-184

  Lorenz, Hanns Martin ^a   Kalden, Joachim R ^a  

^a UNIVERSITY OF ERLANGEN NUREMBERG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIRHEUMATIC AGENT; METHOTREXATE; TUMOR NECROSIS FACTOR ALPHA ANTIBODY;

PRIORITY JOURNAL; REVIEW; RHEUMATIC DISEASE; RHEUMATOID ARTHRITIS;

ANIMALS; ANTIBODIES, MONOCLONAL; ANTIGENS, CD4; ANTIRHEUMATIC AGENTS; DRUG THERAPY, COMBINATION; HUMANS; INTERLEUKIN-10; INTERLEUKIN-4; METHOTREXATE; RHEUMATIC DISEASES; TUMOR NECROSIS FACTOR-ALPHA;

EID: 0032996860     PISSN: 10408711     EISSN: None     Source Type: Journal    
DOI: 10.1097/00002281-199905000-00005     Document Type: Review

References (31)

1. 1 van der Putte L, van Riel P, den Broeden A, Sander O, Rau R, Binder C, et al.: A single dose placebo-controlled phase I study of the fully human anti-TNF antibody D2E7 in patients with rheumatoid arthritis. Arthritis Rheum 1998, 41(suppl):57.
2. 2 Rau R, Sander O, den Broeder A, van Riel P, van der Putte L, Krüger K, et al.: Long-term efficacy and tolerability of multiple i.v. doses of the fully human anti-TNF antibody D2E7 in patients with rheumatoid arthritis. Arthritis Rheum 1998, 41(suppl):55.
3. 3 Schattenkirchner M, Krüger K, Sander O, Rau R, Kroot EJ, van Riel P, et al.: Efficacy and tolerability of weekly subcutaneous injections of the fully human anti-TNF antibody D2E7 in patients with rheumatoid arthritis. Arthritis Rheum 1998, 41(suppl):57.
4. 4 Moreland LW, Baumgartner SW, Schiff MH, Tindall EA, Fleischmann RM, Weaver AL, et al.: Optimal dose of TNF receptor p75 Fc fusion protein (TNFR:FC, Enbrel). Arthritis Rheum 1998, 41(suppl):59.
5. 5 Wendling D, Racadot E, Wijdenes J: Treatment of severe rheumatoid arthritis by anti-interleukin 6 monoclonal antibody. J Rheumatol 1993, 20(2):259-262.
6. 6 Matsuno H, Sawai T, Nezuka T, Uzuki M, Tsuji H, Nishimoto N, Yoshizaki K: Treatment of rheumatoid arthritis with anti-reshaping human interleukin-6 receptor monoclonal antibody. Arthritis Rheum 1998, 41:2014-2021. Elegant work establishing in vivo efficacy of the new IL-6 mAb. The agent was administered intraperitoneally once a week for 4 weeks into SCID mice carrying human RA synovial tissue. By several lines of evidence, the authors show in vivo anti-inflammatory potency of this new biologic compound.
7. 7 Elliott MJ, Maini RN, Feldmann M, Long-Fox A, Charles P, et al.: Repeated therapy wtih monoclonal antibody to tumour necrosis factor alpha (cA2) in patients with rheumatoid arthritis. Lancet 1994, 344:1125-1127.
8. 8 Maini RV, Breedveld FC, Kalden JR, Smolen JS, Davis D, Macfarlane JD, et al.: Therapeutic efficacy of multiple intravenous infusions of anti-tumor necrosis factor α monoclonal antibody combined with low-dose weekly methotrexate in rheumatoid arthritis. Arthritis Rheum 1998, 41:1552-1563. This is the first full article reporting results on combination therapy of the chimeric TNF-α mAb cA2 with MTX as the DMARD being considered as the gold standard in the treatment of patients with RA. Especially in the low-dose cA2 group (1 mg/kg) synergistic effects of cA2 and MTX were evident. One of the possible explanations for this synergism might be inhibition of human antichimeric antibodies formation by B-cell immunosuppression through MTX.
9. 9 Morgan A, Hale G, Waldmann H, Emry P, Isaacs J: Prolonged combination therapy of RA using CD4 and TNF-a blockade: a pilot study. Arhtritis Rheum 1998, 41(suppl):55.
10. 10 Kremer JM: Combination therapy with biologic agents in rheumatoid arthritis: perils and promise. Arthritis Rheum 1998, 41:1548-1551.
11. 11 Lorenz HM, Kalden JR: Biological drugs in rheumatoid arthritis: which ones could be used in combination? BioDrugs 1998, 9:303-324.
12. 12 Yocum DE, Solinger AM, Tesser J, Gluck O, Cornett M, O'Sullivan F, et al.: Clinical and immunologic effects of a primatized anti-CD4 monoclonal antibody in active rheumatoid arthritis: results of a phase I, single dose, dose escalating trial. J Rheumatol 1998, 25:1257-1262.
13. 13 Jorgensen C, Mason U, Baton F, Elliott M, Jackson M, Sany J: Eleven months clinical safety follow-up in RA patients with CD4 lymphopenia following treatment with the primatized anti-CD4 monoclonal antibody, Keliximab. Arthritis Rheum 1998, 41(suppl):56.
14. 14 Panayi GS, Choy EHS, Emery P, Madden S, Breedveld FC, Kraan MC, et al.: Repeat cycle study of high-dose intravenous 4162W94 anti-CD4 monoclonal antibody in rheumatoid arthritis. Arthritis Rheum 1998, 41(suppl):56.
15. 15 Wendling D, Racadot E, Wijdenes J, Sibilia J, Flipo RM, Cantagrel A, et al.: A randomized, double-blind, placebo-controlled multicenter trial of murine anti-CD4 monoclonal antibody therapy in rheumatoid arthritis. J Rheumatol 1998, 25:1457-1461.
16. 16 Moreland LW, Haverty TP, Wacholtz MC, Knowles RW, Bucy RP, Heck LW, Koopman WJ: Nondepleting humanized anti-CD4 monoclonal antibody in patients with refractory rheumatoid arthritis. J Rheumatol 1998, 25:221-228.
17. 17 Moreland LW, Morgan EE, Adamson TC, Fronek Z, Calabrese LH, Cash JM, et al.: T cell receptor peptide vaccination in rheumatoid arthritis: a placebo-controlled trial using a combination of Vb3, Vb14 and Vb17 peptides. Arthritis Rheum 1998, 41:1919-1929. This article provides evidence that vaccination and immunostimulation against T-cell receptor β chains thought to be involved in the pathogenesis or perpetuation of RA might be a new way of treatment for the future.
18. 18 Jorgensen C, Apparailly F, Couret I, Canovas F, Jacquet C, Sany J: Interleukin-4 and interleukin-10 are chondroprotective and decrease mononuclear cell recruitment in human rheumatoid synovium in vivo. Immunology 1998, 93:518-523. In the model with RA synovial tissue coimplanted on human cartilage into SCID mice, IL-4, IL-10, both cytokines, or TNF-α were injected on a regular basis. IL-4 and IL-10 could inhibit cartilage degradation without additive effects. IL-10, but not IL-4, could decrease adhesion molecule expression and cellular invasion into the synovial tissue.
19. 19 van den Bosch F, Russel A, Chir B, Keystone EC, Moreland LW, St. Clair EW, et al.: rhulL-4 in subjects with active rheumatoid arthritis: a phase I dose escalating savety study. Arthritis Rheum 1998, 41(suppl):56.
20. 20 Tak PP, 't Hart BA, Kraan MC, Jonker M, Breedveld FC: The effects of interferon β treatment on arthritis. Arthritis Rheum 1998, 41(suppl):56.
21. 21 Smeets TJM, Kraan MC, Versendaal H, Breedveld FC, Tak PP: Synovial tissue response to IFN-B treatment in RA patients. Arthritis Rheum 1998, 41(suppl):56.
22. 22 Oppenheimer-Marks N, Brezinschek RI, Mohamadzadeh M, Vita R, Lipsky PE: Interleukin-15 is produced by endothelial cells and increases the transendothelial migration of T cells in vitro and in the SCID mouse-human rheumatoid arthritis model in vivo. J Clin Invest 1998, 101:1261-1272.
23. 23 Ruchatz H, Leung BP, Wei XQ, McInnes IB, Liew FY: Soluble IL-15 receptor alpha-chain administration prevents murine collagen-induced arthritis: a role for IL-15 in development of antigen-induced immunopathology. J Immunol 1998, 160:5654-5660. The administration of a soluble fragment of the IL-15 receptor α-chain into DBA/1 mice could effectively suppress development of collagen-induced arthritis. This new therapeutic strategy should encourage further testing in different mouse models and-if effectiveness is confirmed-in humans.
24. 24 Walmsley M, Butler DM, Marinova-Mutafchieva L, Feldmann M: An anti-inflammatory role for interleukin-11 in established murine collagen-induced arthritis. Immunology 1998, 95:31-37. Another anti-inflammatory cytokine, shown in this article to effectively diminish established collagen-induced arthritis. The data suggest that IL-11 is a candidate therapeutic molecule for human inflammatory diseases. The authors' own experience in patients with thrombocytopenia after chemotherapy indicates that pulmonary edema that occurs with high-dose IL-11 treatment might be a limiting factor.
25. 25 Hoffmann JC, Herklotz C, Zeidler H, Bayer B, Westermann J: Anti-CD2 (OX34) MoAb treatment of adjuvant arthritic rats: attenuation of established arthritis, selective depletion of CD4+ T cells, and CD2 downmodulation. Clin Exp Immunol 1997, 110:63-71. Treatment of rats after establishment of adjuvant-induced arthritis with CD2 mAb Ox34 not only led to improvement of disease but-although binding to CD8+ T cells-specifically reduced CD4+ T-cell numbers, suggesting a particular signal in CD4+ T cells.
26. 26 Sakai K, Matsuno H, Morita I, Nezuka T, Tsuji H, Shirai T, et al.: Potential withdrawal of rheumatoid synovium by the induction of apoptosis using a novel in vivo model of rheumatoid arthritis. Arthritis Rheum 1998, 41:1251-1257. This is the first report of an anti-inflammatory effectiveness of Fas/APO-1 mAb in vivo in SCID mice again being implanted with rheumatoid synovial tissue on human cartilage. The mAb was injected intraperitoneally 6 weeks after engraftment. Thirty-six hours after injection, diffuse apoptotic changes were observed in the grafted synovia; 4 weeks after injection, rheumatoid synovial tissue had disappeared.
27. 27 Fridkis-Hareli M, Rosloniec EF, Fugger L, Strominger JL: Synthetic amino acid copolymers that bind to HLA-DR proteins and inhibit type II collagen-reactive T cell clones. Proc Natl Acad Sci U S A 1998, 95:12528-12531. This report indicates that manipulation of antigen presentation might be a new way of more specifically interfere with pathogenetic mechanisms in disease. In vivo studies with the copolymers need to be awaited to judge effectiveness of these reagents in an in vivo situation.
28. 28 del Rosso M, Fibbi G, Pucci M, Matucci Cerinic M: Antisense oligonucleotides against the urokinase receptors: a therapeutic strategy for the control of cell invasion in rheumatoid arthritis and cancer. Clin Exp Rheumatol 1998, 16:389-393.
29. This is an excellent review on the role of matrix metalloproteinases and the serine proteases in a variety of biologic processes important for induction of inflammation and tumorigenesis. Inhibitors of these early and central mediators should be effective in the control of inflammation. In vivo studies must prove feasibility and effectiveness of antisense oligonucleotide treatment.
30. 29 Fibbi G, Pucci M, Serni U, Matuicci Cerinic M, del Rosso M: Antisense targeting of the urokinase receptor blocks urokinase-dependent proliferation, chemoinvasion and chemotaxis of human synovial cells and chondrocytes. Proc Assoc Am Phys 1998, 110:1-11.
31. Targeting the urokinase receptor with an antisense oligonucleotide blocked the urokinase-type plasminogen activator-dependent synoviocyte and chondrocyte proliferation and chemoinvasion in vitro.