Molecular targets in immune-mediated diseases: focus on rheumatoid arthritis

Bibliography

• FELDMANN M, MAINI RN: Anti-TNF a therapy of rheumatoid arthritis: what have we learned? Annu. Rev. Immunol (2001) 19:163–196.
   Google Scholar
• •A review of anti-TNF-a therapy in RA.
   Google Scholar
• LEE DM, WEINBLATT ME: Rheumatoid arthritis. Lancet (2001) 358(9285):903–911.
   PubMed Web of Science ®Google Scholar
• VAN DEN BERG WB: Uncoupling of inflammatory and destructive mechanisms in arthritis. Semin. Arthritis Rheum. (2001) 30(5 Suppl. 2):7–16.
   Google Scholar
• DAOUD KF, JACKSON CG, WILLIAMS HJ: Basic therapy for rheumatoid arthritis: nonsteroidal anti-inflammatory drugs. Compr. The]: (1999) 25(8-10):427–433.
   PubMedGoogle Scholar
• TEN WOLDE S, HERMANS J, BREEDVELD FC, DIJKMANS BA: Effect of resumption of second line drugs in patients with rheumatoid arthritis that flared up after treatment discontinuation. Ann. Rheum. Dis. (1997) 56(4):235–239.
   PubMed Web of Science ®Google Scholar
• PALLADINO MA, BAHJAT FR, THEODORAKIS EA, MOLDAWER LL: Anti-TNF-a therapies: the next generation. Nat. Rev Drug Discov. (2003) 2(9):736–746.
   PubMed Web of Science ®Google Scholar
• •A review of future anti-TNF-a therapies in RA.
   Google Scholar
• FELSON DT, ANDERSON JJ, BOERS M et al.: American College of Rheumatology. Preliminary definition of improvement in rheumatoid arthritis. Arthritis Rheum. (1995) 38(6):727–735.
   PubMed Web of Science ®Google Scholar
• ELLIOTT MJ, MAINI RN, FELDMANN M et al.: Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor a (cAZ) versus placebo in rheumatoid arthritis. Lancet (1994) 344(8930):1105–1110.
   PubMed Web of Science ®Google Scholar
• MAINI RN, BREEDVELD FC, KALDEN JR et al.: Therapeutic efficacy of multiple intravenous infusions of anti-tumor necrosis factor a monoclonal antibody combined with low-dose weekly methotrexate in rheumatoid arthritis. Arthritis Rheum. (1998) 41(9):1552–1563.
   PubMed Web of Science ®Google Scholar
• MORELAND LW, BAUMGARTNER SW, SCHIFF MH et al.: Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75)-Fc fusion protein. N Engl. I Med. (1997) 337(3):141–147.
   PubMed Web of Science ®Google Scholar
• WEINBLATT ME, KREMER JM, BANKHURST AD et al.: A trial of etanercept, a recombinant tumor necrosis factor receptor:Fc fusion protein, in patients with rheumatoid arthritis receiving methotrexate. N Engl. J. Med. (1999) 340(4):253–259.
   PubMed Web of Science ®Google Scholar
• WEINBLATT ME, KEYSTONE EC, FURST DE et al.: Adalimumab, a fully human anti-tumor necrosis factor a monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: the ARMADA trial. Arthritis Rheum. (2003) 48(1):35–45.
   PubMed Web of Science ®Google Scholar
• LIPSKY PE, VAN DER HEIJDE DM, ST CLAIR EW et al.: Infliximab and methotrexate in the treatment of rheumatoid arthritis. Anti-Tumor Necrosis Factor Trial in Rheumatoid Arthritis with Concomitant Therapy Study Group. N Engl. I Med. (2000) 343(22):1594–1602.
   Google Scholar
• BATHON JM, MARTIN RW, FLEISCHMANN RM et al.: A comparison of etanercept and methotrexate in patients with early rheumatoid arthritis. N Engl. I Med. (2000) 343(22):1586–1593.
   PubMed Web of Science ®Google Scholar
• PRESENT DH, RUTGEERTS P, TARGAN S et al.: Infliximab for the treatment of fistulas in patients with Crohn's disease. N Engl. I Med. (1999) 340(18):1398–1405.
   PubMed Web of Science ®Google Scholar
• CHAUDHARI U, ROMANO P, MULCAHY LD et al.: Efficacy and safety of infliximab monotherapy for plaque-type psoriasis: a randomised trial. Lancet (2001) 357(9271):1842–1847.
   PubMed Web of Science ®Google Scholar
• SIEPERJ, BRAUN J: New treatment options in ankylosing spondylitis: a role for anti-TNFa therapy. Ann. Rheum. Dis. (2001) 60\(Suppl. 3):i1158–61.
   Google Scholar
• MEASE PJ: Cytokine blockers in psoriatic arthritis. Ann. Rheum. Dis. (2001) 60\(Suppl. 3):iii37–40.
   Google Scholar
• LOVELL DJ, GIANNINI EH, REIFF A et al.: Etanercept in children with polyarticular juvenile rheumatoid arthritis. Pediatric Rheumatology Collaborative Study Group. N Engl. I Med. (2000) 342(11):763–769.
   PubMed Web of Science ®Google Scholar
• LOVELL DJ, GIANNINI EH, REIFF A et al.: Long-term efficacy and safety of etanercept in children with polyarticular-course juvenile rheumatoid arthritis: interim results from an ongoing multicenter, open-label, extended-treatment trial. Arthritis Rheum. (2003) 48(1):218–226.
   PubMed Web of Science ®Google Scholar
• SKURKOVICH S, BOIKO A, BELIAEVA I et al.: Randomized study of antibodies to IFN-y and TNF-a in secondary progressive multiple sclerosis. Mult. Scler. (2001) 7(5):277–284.
   PubMedGoogle Scholar
• FIRESTEIN GS: Evolving concepts of rheumatoid arthritis. Nature (2003) 423(6937):356–361.
   PubMed Web of Science ®Google Scholar
• BRESNIHAN B, ALVARO-GRACIA JM, COBBY M et al: Treatment of rheumatoid arthritis with recombinant human interleukin-1 receptor antagonist. Arthritis Rheum. (1998) 41(12):2196–2204.
   PubMed Web of Science ®Google Scholar
• JIANG Y, GENANT HK, WATT I et al.: A multicenter, double-blind, dose-ranging, randomized, placebo-controlled study of recombinant human interleukin-1 receptor antagonist in patients with rheumatoid arthritis: radiologic progression and correlation of Genant and Larsen scores. Arthritis Rheum. (2000) 43(5):1001–1009.
   PubMed Web of Science ®Google Scholar
• COHEN S, HURD E, CUSH J et al: Treatment of rheumatoid arthritis with anakinra, a recombinant human interleukin-1 receptor antagonist, in combination with methotrexate: results of a twenty-four-week, multicenter, randomized, double-blind, placeboHcontrolled trial. Arthritis Rheum. (2002) 46(3):614–624.
   PubMed Web of Science ®Google Scholar
• BUCH MH, BINGHAM SJ, SETO Y et al.: Lack of response to anakinra in rheumatoid arthritis following failure of tumor necrosis factor a blockade. Arthritis Rheum. (2004) 50(3):725–728.
   PubMedGoogle Scholar
• ••A study showing that patientsunresponsive to TNF blockade were also unresponsive to IL-1 blockade.
   Google Scholar
• ZWERINA J, HAYER S, TOHIDAST-AKRAD M et al.: Single and combined inhibition of tumor necrosis factor, interleukin-1, and RANKL pathways in tumor necrosis factor-induced arthritis: effects on synovial inflammation, bone erosion, and cartilage destruction. Arthritis Rheum. (2004) 50(1):277–290.
   PubMed Web of Science ®Google Scholar
• WALSH DA, HAY WOOD L: Angiogenesis: a therapeutic target in arthritis. CLIFF. Opin. Investig. Drugs (2001) 2(8):1054–1063.
   PubMedGoogle Scholar
• ABRAMSON SB, AMIN A: Blocking the effects of IL-1 in rheumatoid arthritis protects bone and cartilage. Rheumatology (2002) 41(9):972–980.
   PubMed Web of Science ®Google Scholar
• CHOY EH, ISENBERG DA, GARROOD T et al.: Therapeutic benefit of blocking interleukin-6 activity with an anti-interleukin-6 receptor monoclonal antibody in rheumatoid arthritis: a randomized, double-blind, placebo-controlled, dose-escalation trial. Arthritis Rheum. (2002) 46(12):3143–3150.
   PubMed Web of Science ®Google Scholar
• •A study demonstrating the efficacy of IL-6 blockade in the treatment of RA.
   Google Scholar
• VANDENBROECK K, ALLOZA I, GADINA M, MATTHYS P: Inhibiting cytokines of the interleukin-12 family: recent advances and novel challenges. Pharm. Pharmacol (2004) 56(2):145–160.
   PubMed Web of Science ®Google Scholar
• KIM TS, KANG BY, LEE MH, CHOE YK, HVVANG SY: Inhibition of interleukin-12 production by auranofin, an anti-rheumatic gold compound, deviates CD4(-1-) T cells from the Thl to the Th2 pathway. Br: J. Pharmacol (2001) 134(3):571–578.
   PubMed Web of Science ®Google Scholar
• KANG BY, CHUNG SW, IM SY, CHOE YK, KIM TS: Sulfasalazine prevents T-helper 1 immune response by suppressing interleukin-12 production in macrophages. Immunology (1999) 98(1):98–103.
   PubMed Web of Science ®Google Scholar
• KANG BY, CHUNG SW, KIM SH et al:Retinoid-mediated inhibition of interleukin-12 production in mouse macrophages suppresses Thl cytokine profile in CD4(+) T cells. Br. J. Pharmacol (2000) 130(3):581–586.
   PubMed Web of Science ®Google Scholar
• BUTLER DM, MALFAIT AM, MAINI RN, BRENNAN FM, FELDMANN M: Anti-IL-12 and anti-TNF antibodies synergistically suppress the progression of murine collagen-induced arthritis. Eur. I Immunol (1999) 29(7):2205–2212.
   PubMed Web of Science ®Google Scholar
• MURPHY CA, LANGRISH CL, CHEN Y et al.: Divergent pro- and antiinflammatory roles for IL-23 and IL-12 in joint autoimmune inflammation. J. Exp. Med. (2003) 198(12):1951–1957.
   PubMed Web of Science ®Google Scholar
• •A study showing that it is IL-23, and not IL-12, that is important for murine arthritis development.
   Google Scholar
• STROM TB, KELLEY VR, MURPHY JR, NICHOLS J, WOODWORTH TG: Interieukin-2 receptor-directed therapies: antibody- or cytokine-based targeting molecules. Anna. Rev. Med. (1993) 44:343–353.
   PubMed Web of Science ®Google Scholar
• MORELAND LW, SEWELL KL, TRENTHAM DE et al.: Interleukin-2 diphtheria fusion protein (DAB486IL-2) in refractory rheumatoid arthritis. A double-blind, placebo-controlled trial with open-label extension. Arthritis Rheum. (1995) 38(9):1177–1186.
   PubMed Web of Science ®Google Scholar
• GOTTLIEB SL, GILLEAUDEAU P, JOHNSON R et al.: Response of psoriasis to a lymphocyte-selective toxin (DAB389IL-2) suggests a primary immune, but not keratinocyte, pathogenic basis. Nat. Med. (1995) 1(5):442–447.
   PubMed Web of Science ®Google Scholar
• RUCHATZ H, LEUNG BP, WEI XQ, MCINNES IB, LIEW FY: Soluble IL-15 receptor a-chain administration prevents murine collagen-induced arthritis: a role for IL-15 in development of antigen-induced immunopathology.j. Immunol (1998) 160(11):5654–5660.
   Google Scholar
• LIEW FY, MCINNES IB: Role of interleukin 15 and interleukin 18 in inflammatory response. Ann. Rheum. Dis. (2002) 61\(Suppl. 2):ii100–102.
   Google Scholar
• STAMP LK, JAMES MJ, CLELAND LG: Interleukin-17: the missing link between T-cell accumulation and effector cell actions in rheumatoid arthritis? Immunol. Cell Biol. (2004) 82(1):1–9.
   Google Scholar
• NAKAE S, SAIJO S, HORAI R et al.: IL-17 production from activated T cells is required for the spontaneous development of destructive arthritis in mice deficient in IL-1 receptor antagonist. Proc. Nati Acad. Sci. USA (2003) 100(10):5986–5990.
   PubMed Web of Science ®Google Scholar
• LUBBERTS E, KOENDERS MI, OPPERS-WALGREEN B et al: Treatment with a neutralizing anti-murine interleukin-17 antibody after the onset of collagen-induced arthritis reduces joint inflammation, cartilage destruction, and bone erosion. Arthritis Rheum. (2004) 50(2):650–659.
   PubMed Web of Science ®Google Scholar
• JOVANOVIC DV, DI BATTISTA JA, MARTEL-PELLETIER J et al.: Modulation of TIMP-1 synthesis by antiinflammatory cytokines and prostaglandin E2 in interleukin 17 stimulated human monocytes/macrophages. Rheumatol (2001) 28(4):712–718.
   Web of Science ®Google Scholar
• CHABAUD M, MIOSSEC P: The combination of tumor necrosis factor a blockade with interleukin-1 and interleukin-17 blockade is more effective for controlling synovial inflammation and bone resorption in an ex vivo model. Arthritis Rheum. (2001) 44(6):1293–1303.
   PubMedGoogle Scholar
• GRACIE JA, FORSEY RJ, CHAN WL et al: A proinflammatory role for IL-18 in rheumatoid arthritis. I Clin. Invert. (1999) 104(10):1393–1401.
   PubMed Web of Science ®Google Scholar
• SUGAYA M, NAKAMURA K, TAMAKI K: Interleukins 18 and 12 synergistically upregulate interferon-y production by murine dendritic epidermal T cells. Invest. Dermatol (1999) 113(3):350–354.
   PubMed Web of Science ®Google Scholar
• WEI XQ, LEUNG BP, ARTHUR HM, MCINNES IB, LIEW FY: Reduced incidence and severity of collagen-induced arthritis in mice lacking IL-18. J. Immunol (2001) 166(1):517–521.
   PubMed Web of Science ®Google Scholar
• PLATER-ZYBERK C, JOOSTEN LA, HELSEN MM et al.: Therapeutic effect of neutralizing endogenous IL-18 activity in the collagen-induced model of arthritis. Clin. Invest. (2001) 108(12):1825–1832.
   Google Scholar
• SMEETS RL, VAN DE LOO FA, ARNTZ OJ et al.: Adenovical delivery of IL-18 binding protein C ameliorates collagen-induced arthritis in mice. Gene Ther. (2003) 10(12):1004–1011.
   Google Scholar
• LOCHNER M, FORSTER I: Anti-interleukin-18 therapy in murine models of inflammatory bowel disease. Pathobiology (2002) 70(3):164–169.
   PubMed Web of Science ®Google Scholar
• KANAI T, URAUSHIHARA K, TOTSUKA T et al.: Macrophage-derived IL-18 targeting for the treatment of Crohn's disease. Carr. Drug Targets Inflamm. Allergy (2003) 2(2):131–136.
   PubMedGoogle Scholar
• HAMILTON JA: GM-CSF in inflammation andautoimmunity. Trends Immunol. (2002) 23(8):403–408.
   PubMed Web of Science ®Google Scholar
• •Review of GM-CSF and its role in inflammation.
   Google Scholar
• CAMPBELL IK, RICH MJ, BISCHOF RJ et al.: Protection from collagen-induced arthritis in granulocyte-macrophage colony-stimulating factor-deficient mice. Immunol (1998) 161(7):3639–3644.
   Web of Science ®Google Scholar
• YANG YH, HAMILTON JA: Dependence of interleukin- 1-induced arthritis on granulocyte-macrophage colony-stimulating factor. Arthritis Rheum. (2001) 44(1):111–119.
   PubMedGoogle Scholar
• COOK AD, BRAINE EL, CAMPBELL IK, RICH MJ, HAMILTON JA: Blockade of collagen-induced arthritis post-onset by antibody to granulocyte-macrophage colony-stimulating factor (GM-CSF): requirement for GM-CSF in the effector phase of disease. Arthritis Res. (2001) 3(5):293–298.
   PubMedGoogle Scholar
• MCQUALTER JL, DARWICHE R, EWING C et al.: Granulocyte macrophage colony-stimulating factor: a new putative therapeutic target in multiple sclerosis. J. Exp. Med. (2001) 194(7):873–882.
   PubMed Web of Science ®Google Scholar
• KITCHING AR, RU HUANG X, TURNER AL et al.: The requirement for granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in leukocyte-mediated immune glomerular injury." Am. Soc. Nephrol (2002) 13(2):350–358.
   Google Scholar
• BOZINOVSKI S, JONES JE, VLAHOS R, HAMILTON JA, ANDERSON GP: Granulocyte/macrophage colony-stimulating factor (GM-CSF) regulates lung innate immunity to lipopolysaccharide through Akt/Erk activation of NFicB and AP-1 in vivo. J. Biol. Chem. (2002) 277(45):42808–42814.
   PubMed Web of Science ®Google Scholar
• BOZINOVSKI S, JONES J, BEAVITT SJ et al.: Innate immune responses to LPS in mouse lung are suppressed and reversed by neutralization of GM-CSF via repression of TLR-4. Am. I Physiol Lung Cell MM. Physiol (2004) 286(4):L877–L885.
   Web of Science ®Google Scholar
• YANG N, NIKOLIC-PATERSON DJ, NG YY et al.: Reversal of established rat crescentic glomerulonephritis by blockade of macrophage migration inhibitory factor (MIF): potential role of MIF in regulating glucocorticoid production. MM. Med. (1998) 4(6):413–424.
   Google Scholar
• LEECH M, METZ C, SANTOS L et al: Involvement of macrophage migration inhibitory factor in the evolution of rat adjuvant arthritis. Arthritis Rheum. (1998) 41(5):910–917.
   PubMedGoogle Scholar
• DE JONG YP, ABADIA-MOLINA AC, SATOSKAR AR et al.: Development of chronic colitis is dependent on the cytokine MIF. Nat. Litman. (2001) 2(11):1061–1066.
   Web of Science ®Google Scholar
• TARNER IH, NAKAJIMA A, SEROOGY CM et al: Retroviral gene therapy of collagen-induced arthritis by local delivery of IL-4. Clin. Immunol (2002) 105(3):304–314.
   PubMed Web of Science ®Google Scholar
• JOOSTEN LA, LUBBERTS E, DUREZ P et al.: Role of interleukin-4 and interleukin-10 in murine collagen-induced arthritis. Protective effect of interleukin-4 and interleukin-10 treatment on cartilage destruction. Arthritis Rheum. (1997) 40(2):249–260.
   Google Scholar
• MARTIN R: Interleuldn 4 treatment of psoriasis: are pleiotropic cytokines suitable therapies for autoimmune diseases? Trends Pharmacol Sci. (2003) 24(12):613–616.
   Google Scholar
• KEYSTONE E, WHERRY J, GRINT P: IL-10 as a therapeutic strategy in the treatment of rheumatoid arthritis. Rheum. Dis. Clin. North Am. (1998) 24(3):629–639.
   PubMed Web of Science ®Google Scholar
• LI MC, HE SH: IL-10 and its related cytokines for treatment of inflammatory bowel disease. World J. Gastroenterol (2004) 10(5):620–625.
   PubMed Web of Science ®Google Scholar
• BESSIS N, BOISSIER MC, FERRARA P et al.: Attenuation of collagen-induced arthritis in mice by treatment with vector cells engineered to secrete interleukin-13. Ear. Immunol (1996) 26(10):2399–2403.
   PubMed Web of Science ®Google Scholar
• WOODS JM, AMIN MA, KATSCHKE KJ Jr et al.: Interleukin-13 gene therapy reduces inflammation, vascularization, and bony destruction in rat adjuvant-induced arthritis. Hum. Gene The]: (2002) 13(3):381–393.
   Google Scholar
• WOODS JM, KATSCHKE KJ Jr, TOKUHIRA M et al.: Reduction of inflammatory cytokines and prostaglandin E2 by IL-13 gene therapy in rheumatoid arthritis synovium. I Immunol (2000) 165(5):2755–2763.
   PubMed Web of Science ®Google Scholar
• MAEDA T, SAIKAWA I, HOTOKEBUCHI T et al.: Exacerbation of established collagen-induced arthritis in mice treated with an anti-T cell receptor antibody. Arthritis Rheum. (1994) 37(3):406–413.
   PubMedGoogle Scholar
• MORELAND LW, HAVERTY TP, WACHOLTZ MC et al: Nondepleting humanized anti-CD4 monoclonal antibody in patients with refractory rheumatoid arthritis. I Rheumatol (1998) 25(2):221–228.
   Web of Science ®Google Scholar
• SCHULZE-KOOPS H, DAVIS LS, HAVERTY TP, WACHOLTZ MC, LIPSKY PE: Reduction of Thl cell activity in the peripheral circulation of patients with rheumatoid arthritis after treatment with a non-depleting humanized monoclonal antibody to CD4. Rheumatol (1998) 25(11):2065–2076.
   Web of Science ®Google Scholar
• UTSET TO, AUGER JA, PEACE D et al:Modified anti-CD3 therapy in psoriatic arthritis: a Phase I/II clinical trial. Rheumatol (2002) 29(9):1907–1913.
   Web of Science ®Google Scholar
• MATTESON EL, YOCUM DE, ST CLAIR EW et al.: Treatment of active refractory rheumatoid arthritis with humanized monoclonal antibody CAMPATH-1H administered by daily subcutaneous injection. Arthritis Rheum. (1995) 38(9):1187–1193.
   Google Scholar
• BRETT SJ, BAXTER G, COOPER H et al.: Emergence of CD52-, glycosylphosphatidylinositol-anchor-deficient lymphocytes in rheumatoid arthritis patients following CAMPATH-1H treatment. Int. batman& (1996) 8(3):325–334.
   Google Scholar
• BRETT S, BAXTER G, COOPER H et al: Repopulation of blood lymphocyte sub-populations in rheumatoid arthritis patients treated with the depleting humanized monoclonal antibody, CAMPATH-1H. Immunology (1996) 88(1):13–19.
   PubMed Web of Science ®Google Scholar
• MALEK TR: The main function of IL-2 is to promote the development of T regulatory cells. Leukoc. Biol. (2003) 74(6):961–965.
   PubMed Web of Science ®Google Scholar
• BANERJEE S, WEI BY, HILLMAN K, LUTHRA HS, DAVID CS: Immunosuppression of collagen-induced arthritis in mice with an anti-IL-2 receptor antibody. J. Immunol (1988) 141(4):1150–1154.
   PubMed Web of Science ®Google Scholar
• MORGAN ME, SUTMULLER RP, WITTEVEEN HJ et al: CD25+ cell depletion hastens the onset of severe disease in collagen-induced arthritis. Arthritis Rheum. (2003) 48(5):1452–1460.
   PubMedGoogle Scholar
• SLAVIK JM, HUTCHCROFT JE, BIERER BE: CD28/CTLA-4 and CD80/CD86 families: signaling and function. Immunol Res. (1999) 19(1):1–24.
   PubMed Web of Science ®Google Scholar
• MORELAND LW, ALTEN R, VAN DEN BOSCH F et al.: Costimulatory blockade in patients with rheumatoid arthritis: a pilot, dose-finding, double-blind, placebo-controlled clinical trial evaluating CTLA-41g and LEA29Y eighty-five days after the first infusion. Arthritis Rheum. (2002) 46(6):1470–1479.
   Google Scholar
• KREMER JM, WESTHOVENS R, LEON M et al.: Treatment of rheumatoid arthritis by selective inhibition of T-cell activation with fusion protein CTLA4Ig. N. Engl. J. Med. (2003) 349(20):1907–1915.
   PubMed Web of Science ®Google Scholar
• SCHONBECK U, LIBBY P: The CD40/CD154 receptor/ligand dyad. Cell. MM. Life ScL (2001) 58(b):4–43.
   Google Scholar
• DAIKH DI, WOFSY D: Treatment of autoimmunity by inhibition of T cell costimulation. Adv. Exp. Med. Biol. (2001) 490:113–117.
   PubMed Web of Science ®Google Scholar
• YOSHINAGA SK, WHORISKEY JS, KHARE SD et al.: T-cell co-stimulation through B7RP-1 and ICOS. Nature (1999) 402(6763):827–832.
   PubMed Web of Science ®Google Scholar
• NURIEVA RI, TREUTING P, DUONGJ, FLAVELL RA, DONG C: Inducible costimulator is essential for collagen-induced arthritis. I Clin. Invest. (2003) 111(5):701–706.
   PubMed Web of Science ®Google Scholar
• IWAI H, KOZONO Y, HIROSE S et al: Amelioration of collagen-induced arthritis by blockade of inducible costimulator-B7 homologous protein costimulation. Immunol (2002) 169(8):4332–4339.
   Web of Science ®Google Scholar
• ROTTMAN JB, SMITH T, TONRA JR et al.: The costimulatory molecule ICOS plays an important role in the immunopathogenesis of EAE. Nat. Immunol (2001) 2(7):605–611.
   PubMed Web of Science ®Google Scholar
• GONZALO JA, TIAN J, DELANEY T et al.:ICOS is critical for T helper cell-mediated lung mucosal inflammatory responses. Nat. Immunol (2001) 2(7):597–604.
   PubMed Web of Science ®Google Scholar
• YAMAZAKI T, AKIBA H, IWAI H et al: Expression of programmed death 1 ligands by murine T cells and APC. I Immunol (2002) 169(10):5538–5545.
   PubMed Web of Science ®Google Scholar
• NISHIMURA H, NOSE M, HIAI H, MINATO N, HONJO T: Development of lupus-like autoimmune diseases by disruption of the PD-1 gene encoding an ITIM motif-carrying immunoreceptor. Immunity (1999) 11(2):141–151.
   PubMed Web of Science ®Google Scholar
• OKAZAKI T, IWAI Y, HONJO T: New regulatory co-receptors: inducible co-stimulator and PD-1. Curt: Opin. Immunol (2002) 14(6):779–782.
   PubMed Web of Science ®Google Scholar
• BROWN JA, DORFMAN DM, MA FR et al.: Blockade of programmed death-1 ligands on dendritic cells enhances T cell activation and cytokine production. Immunol (2003) 170(3):1257–1266.
   Web of Science ®Google Scholar
• KANAI T, TOTSUKA T, URAUSHIHARA K et al: Blockade of B7-H1 suppresses the development of chronic intestinal inflammation. I Immunol (2003) 171(8):4156–4163.
   PubMed Web of Science ®Google Scholar
• DE VITA S, ZAJA F, SACCO S et al: Efficacy of selective B cell blockade in the treatment of rheumatoid arthritis: evidence for a pathogenetic role of B cells. Arthritis Rheum. (2002) 46(8):2029–2033.
   PubMed Web of Science ®Google Scholar
• LEANDRO MJ, EDWARDS JC, CAMBRIDGE G: Clinical outcome in 22 patients with rheumatoid arthritis treated with B lymphocyte depletion. Ann. Rheum. Dis. (2002) 61(10):883–888.
   PubMed Web of Science ®Google Scholar
• VEGA MI, HUERTA-YEPAZ S, GARBAN H et al.: Rituximab inhibits p38-MAPK activity in 2F7 B NHL and decreases IL-10 transcription: pivotal role of p38-MAPK in drug resistance. Oncogene (2004) 23(20):3530–3540.
   PubMed Web of Science ®Google Scholar
• LOONEY RJ, ANOLIK J, SANZ I: B cells as therapeutic targets for rheumatic diseases. Can: Opin. Rheumatol (2004) 16(3):180–185.
   PubMed Web of Science ®Google Scholar
• KAVANAUGH AF, DAVIS LS, NICHOLS LA et al: Treatment of refractory rheumatoid arthritis with a monoclonal antibody to intercellular adhesion molecule 1. Arthritis Rheum. (1994) 37(7):992–999.
   PubMed Web of Science ®Google Scholar
• KAVANAUGH AF, DAVIS LS, JAIN RI et al.: A Phase I/II open label study of the safety and efficacy of an anti-ICAM-1 (intercellular adhesion molecule-1; CD54) monoclonal antibody in early rheumatoid arthritis. I Rheumatol (1996) 23 (8) :1338–1344.
   Web of Science ®Google Scholar
• KAVANAUGH AF, SCHULZE-KOOPS H, DAVIS LS, LIPSKY PE: Repeat treatment of rheumatoid arthritis patients with a murine anti-intercellular adhesion molecule 1 monoclonal antibody. Arthritis Rheum. (1997) 40(5):849–853.
   PubMed Web of Science ®Google Scholar
• ELLIS CN, KRUEGER GG: Treatment of chronic plaque psoriasis by selective targeting of memory effector T lymphocytes. N Engl. I Med. (2001) 345(4):248–255.
   PubMed Web of Science ®Google Scholar
• KRUEGER GG: Selective targeting of T cell subsets: focus on alefacept - a remittive therapy for psoriasis. Expert Opin. Biol. Ther. (2002) 2(4):431–441.
   PubMed Web of Science ®Google Scholar
• DA SILVA AJ, BRICKELMAIER M, MAJEAU GR et al: Alefacept, an immunomodulatory recombinant LFA-3/IgG1 fusion protein, induces CD16 signaling and CD2/CD16-dependent apoptosis of CD2(+) cells. Immunol (2002) 168(9):4462–4471.
   Web of Science ®Google Scholar
• PAPP K, BISSONNETTE R, KRUEGER JG et al.: The treatment of moderate to severe psoriasis with a new anti-CD1 1 a monoclonal antibody. I Am. Acad. Dermatol (2001) 45(5):665–674.
   PubMed Web of Science ®Google Scholar
• TUTRONE WD, KAGEN MH, BARBAGALLO J, WEINBERG JM: Biologic therapy for psoriasis: a brief history, II. Cutts (2001) 68(6):367–372.
   PubMed Web of Science ®Google Scholar
• RAYCHAUDHURI A, CHOU M, WEETALL M, JENG AY: Blockade of integrin VLA-4 prevents inflammation and matrix metalloproteinase expression in a murine model of accelerated collagen-induced arthritis. Inflammation (2003) 27(2):107–113.
   PubMed Web of Science ®Google Scholar
• GORDON FH, HAMILTON MI, DONOGHUE S et al.: A pilot study of treatment of active ulcerative colitis with natalizumab, a humanized monoclonal antibody to a-4 integrin. Aliment. Pharmacol The]: (2002) 16(4):699–705.
   PubMed Web of Science ®Google Scholar
• GHOSH S, GOLDIN E, GORDON FH et al.: Natalizumab for active Crohn's disease. N Engl. I Med. (2003) 348(1):24–32.
   PubMed Web of Science ®Google Scholar
• GORDON FH, LAI CW, HAMILTON MI et al.: A randomized placebo-controlled trial of a humanized monoclonal antibody to a4 integrin in active Crohn's disease. Gastroenterology (2001) 121(2):268–274.
   PubMed Web of Science ®Google Scholar
• TUBRIDY N, BEHAN PO, CAPILDEO R et al: The effect of anti-a4 integrin antibody on brain lesion activity in MS. The UK Antegren Study Group. Neurology (1999) 53(3):466–472.
   PubMed Web of Science ®Google Scholar
• DALTON CM, MISZKIEL KA, BARKER GJ et al.: Effect of natalizumab on conversion of gadolinium enhancing lesions to Ti hypointense lesions in relapsing multiple sclerosis. I Neurol (2004) 251(4):407–413.
   PubMed Web of Science ®Google Scholar
• ALAHARI SK, REDDIG PJ, JULIANO RL: Biological aspects of signal transduction by cell adhesion receptors. Int. Rev Cytol. (2002) 220:145–184.
   PubMedGoogle Scholar
• KONTTINEN YT, AINOLA M, VALLEALA H et al.: Analysis of 16 different matrix metalloproteinases (MMP-1 to MMP-20) in the synovial membrane: different profiles in trauma and rheumatoid arthritis. Ann. Rheum. Dis. (1999) 58(11):691–697.
   PubMed Web of Science ®Google Scholar
• SADOWSKI T, STEINMEYERJ: Effects of tetracyclines on the production of matrix metalloproteinases and plasminogen activators as well as of their natural inhibitors, tissue inhibitor of metalloproteinases-1 and plasminogen activator inhibitor-1. Inflamm. Res. (2001) 50(3):175–182.
   PubMed Web of Science ®Google Scholar
• DEAGE V, BURGER D, DAYER JM: Exposure of T lymphocytes to leflunomide but not to dexamethasone favors the production by monocytic cells of interleukin-1 receptor antagonist and the tissue-inhibitor of metalloproteinases-1 over that of interleukin-lbeta and metalloproteinases. Ear: Cytokine Netw. (1998) 9(4):663–668.
   PubMed Web of Science ®Google Scholar
• HAMADA T, ARIMA N, SHINDO M, SUGAMA K, SASAGURI Y: Suppression of adjuvant arthritis of rats by a novel matrix metalloproteinase-inhibitor. Br. J. Pharmacol. (2000) 131(8):1513–1520.
   PubMed Web of Science ®Google Scholar
• CELIKER MY, RAMAMURTHY N, XU JW et al.: Inhibition of adjuvant-induced arthritis by systemic tissue inhibitor of metalloproteinases 4 gene delivery. Arthritis Rheum. (2002) 46(12):3361–3368.
   PubMed Web of Science ®Google Scholar
• CLOSE DR: Matrix metalloproteinase inhibitors in rheumatic diseases. Ann. Rheum. Dis. (2001) 60\(Suppl. 3):iii62–67.
   Google Scholar
• KEYSTONE E: Treatments no longer in development for rheumatoid arthritis. Ann. Rheum. Dis. (2002) 61\(Suppl. 2):ii43–45.
   Google Scholar
• NEUMANN E, BARNUM SR, TARNER IH et al.: Local production of complement proteins in rheumatoid arthritis synovium. Arthritis Rheum. (2002) 46(4):934–945.
   PubMed Web of Science ®Google Scholar
• WANG Y, ROLLINS SA, MADRI JA, MATIS LA: Anti-05 monoclonal antibody therapy prevents collagen-induced arthritis and ameliorates established disease. Proc. Nati Acad. Sci. USA (1995) 92(19):8955–8959.
   PubMed Web of Science ®Google Scholar
• KAPLAN M: Eculizumab (Alexion). Curr: Opin. Investig. Drugs (2002) 3(7):1017–1023.
   PubMedGoogle Scholar
• SCHNARE M, BARTON GM, HOLT AC et al.: Toll-like receptors control activation of adaptive immune responses. Nat. Immun. (2001) 2(10):947–950.
   Google Scholar
• ••Describes how the innate immunesystem controls activation of the adaptive immune system.
   Google Scholar
• PASARE C, MEDZHITOV R: Toll pathway-dependent blockade of CD4+CD25+ T cell-mediated suppression by dendritic cells. Science (2003) 299(5609):1033–1036.
   PubMed Web of Science ®Google Scholar
• JOOSTEN LA, KOENDERS MI, SMEETS RL et al.: Toll-like receptor 2 pathway drives streptococcal cell wall-induced joint inflammation: critical role of myeloid differentiation factor 88. brimunol. (2003) 171(11):6145–6153.
   Google Scholar
• DENG GM, NILSSON IM, VERDRENGH M, COLLINS LV, TARKOWSKI A: Intra-articularly localized bacterial DNA containing CpG motifs induces arthritis. Nat. Med. (1999) 5(6):702–705.
   PubMed Web of Science ®Google Scholar
• DENG GM, TARKOWSKI A: The features of arthritis induced by CpG motifs in bacterial DNA. Arthritis Rheum. (2000) 43(2):356–364.
   PubMedGoogle Scholar
• YOSHINO S, SASATOMI E, OHSAWA M: Bacterial lipopolysaccharide acts as an adjuvant to induce autoimmune arthritis in mice. Immunology (2000) 99(4):607–614.
   PubMed Web of Science ®Google Scholar
• CHOE JY, CRAIN B, WU SR, CORR M: Interleukin 1 receptor dependence of serum transferred arthritis can be circumvented by toll-like receptor 4 signaling. Exp. Med. (2003) 197(4):537–542.
   PubMed Web of Science ®Google Scholar
• •Shows how TLR signalling can bypass the need for IL-1 in chronic joint inflammation.
   Google Scholar
• BEG AA: Endogenous ligands of toll-like receptors: implications for regulating inflammatory and immune responses. Trends Immunol. (2002) 23(11):509–512.
   PubMed Web of Science ®Google Scholar
• LEADBETTER EA, RIFKIN IR, HOHLBAUM AM et al.: Chromatin-IgG complexes activate B cells by dual engagement of IgM and toll-like receptors. Nature (2002) 416(6881):603–607.
   PubMed Web of Science ®Google Scholar
• ••Describes the role of TLR9 inautoantibody production.
   Google Scholar
• SCHETT G, TOHIDAST-AKRAD M, SMOLEN JS et al.: Activation, differential localization, and regulation of the stress-activated protein kinases, extracellular signal-regulated kinase, c-JUN N-terminal kinase, and p38-mitogen-activated protein kinase, in synovial tissue and cells in rheumatoid arthritis. Arthritis Rheum. (2000) 43(11):2501–2512.
   PubMed Web of Science ®Google Scholar
• ADAMS JL, BADGER AM, KUMAR S, LEE JC: p38-MAP kinase: molecular target for the inhibition of pro-inflammatory cytokines. Frog. Med. Chem. (2001) 38:1–60.
   PubMedGoogle Scholar
• BADGER AM, BRADBEERJN, VOTTA B et al.: Pharmacological profile of SB 203580, a selective inhibitor of cytokine suppressive binding protein/p38 kinase, in animal models of arthritis, bone resorption, endotoxin shock and immune function. Pharmacol. Exp. Ther. (1996) 279(3):1453–1461.
   PubMed Web of Science ®Google Scholar
• BADGER AM, GRISWOLD DE, KAPADIA R et al.: Disease-modifying activity of SB 242235, a selective inhibitor of p38-mitogen-activated protein kinase, in rat adjuvant-induced arthritis. Arthritis Rheum. (2000) 43(1):175–183.
   PubMed Web of Science ®Google Scholar
• COLLIS AJ, FOSTER ML, HALLEY F et al.: RPR203494 a pyrimidine analogue of the p38 inhibitor RPR200765A with an improved M vitro potency. Bioorg. Med. Chem. Lett. (2001) 11(5):693–696.
   PubMed Web of Science ®Google Scholar
• KUMAR S, BOEHM J, LEE JC: p38-MAP kinases: key signalling molecules as therapeutic targets for inflammatory diseases. Nat. Rev Drug Discov. (2003) 2(9):717–726.
   PubMed Web of Science ®Google Scholar
• MINDEN A, KARIN M: Regulation and function of the JNK subgroup of MAP kinases. Biochim. Biophys. Acta (1997) 1333(2):F85–F104.
   Web of Science ®Google Scholar
• HAN Z, BOYLE DL, CHANG L et al.: c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis. Clin. Invest. (2001) 108(1):73–81.
   Google Scholar
• JIMI E, AOKI K, SAITO H et al.: Selective inhibition of NF-icB blocks osteoclastogenesis and prevents inflammatory bone destruction in vivo. Nat. Med. (2004) 10(6):617–624.
   PubMed Web of Science ®Google Scholar
• CLOHISY JC, ROY BC, BIONDO C et al.: Direct inhibition of NF-icB blocks bone erosion associated with inflammatory arthritis. I Immunol. (2003) 171(10):5547–5553.
   PubMed Web of Science ®Google Scholar
• KARIN M, YAMAMOTO Y, WANG QM: The IKK- NF-tPt.- system: a treasure trove for drug development. Nat. Rev Drug Discov. (2004) 3(1):17–26.
   Google Scholar
• •A review on the IKK NF-x13 system and drug targets.
   Google Scholar
• HARRISON LC, HAFLER DA: Antigen-specific therapy for autoimmune disease. Carr: Opin. Immunol. (2000) 12(6):704–711.
   PubMed Web of Science ®Google Scholar
• KITANO H: Systems biology: a brief overview. Science (2002) 295(5560):1662–1664.
   PubMed Web of Science ®Google Scholar
• GRANT EP, PICKARD MD, BRISKIN MJ, GUTIERREZ-RAMOS JC: Gene expression profiles: creating new perspectives in arthritis research. Arthritis Rheum. (2002) 46(4):874–884.
   PubMedGoogle Scholar
• ••A comprehensive review onmicroarray technology and its use in profiling RA patients.
   Google Scholar
• VAN DER POUW KRAAN TC, VAN GAALEN FA, HUIZINGA TW et al.: Discovery of distinctive gene expression profiles in rheumatoid synovium using cDNA microarray technology: evidence for the existence of multiple pathways of tissue destruction and repair. Genes Immun. (2003) 4(3):187–196.
   PubMed Web of Science ®Google Scholar
• CROW MK, WOHLGEMUTH J: Microarray analysis of gene expression in lupus. Arthritis Res. Ther: (2003) 5(6):279–287.
   PubMed Web of Science ®Google Scholar
• WANDINGER KP, STURZEBECHER CS, BIELEKOVA B et al.: Complex immunomodulatory effects of interferon-I3 in multiple sclerosis include the upregulation of T helper 1-associated marker genes. Ann. Neurol. (2001) 50(3):349–357.
   PubMed Web of Science ®Google Scholar
• SAUTER G, SIMON R, HILLAN K: Tissue microarrays in drug discovery. Nat. Rev Drug Discov. (2003) 2(12):962–972.
   PubMed Web of Science ®Google Scholar
• LORENZ P, RUSCHPLER P, KOCZAN D, STIEHL P, THIESEN HJ: From transcriptome to proteome: differentially expressed proteins identified in synovial tissue of patients suffering from rheumatoid arthritis and osteoarthritis by an initial screen with a panel of 791 antibodies. Proteomics (2003) 3 (6) :991–1002.
   PubMed Web of Science ®Google Scholar
• AEBERSOLD R, MANN M: Mass spectrometry-based proteomics. Nature (2003) 422(6928):198–207.
   PubMed Web of Science ®Google Scholar
• SINZ A, BANTSCHEFF M, MIKKAT S et al.: Mass spectrometric proteome analyses of synovial fluids and plasmas from patients suffering from rheumatoid arthritis and comparison to reactive arthritis or osteoarthritis. Electrophoresis (2002) 23 (19):3445–3456.
   PubMed Web of Science ®Google Scholar
• TEMPLIN ME STOLL D, SCHRENK M et al.: Protein microarray technology. Drug Discov. Today (2002) 7(15):815–822.
   Google Scholar
• LUEKING A, HORN M, EICKHOFF H et al.: Protein microarrays for gene expression and antibody screening. Anal. Biochem. (1999) 270(1):103–111.
   PubMed Web of Science ®Google Scholar
• WALTER G, BUSSOW K, CAHILL D, LUEKING A, LEHRACH H: Protein arrays for gene expression and molecular interaction screening. CLIFF. Opin. Microbiol. (2000) 3 (3):298–302.
   PubMed Web of Science ®Google Scholar
• PAULUS HE, EGGER MJ, WARD JR, WILLIAMS HJ: Analysis of improvement in individual rheumatoid arthritis patients treated with disease-modifying antirheumatic drugs, based on the findings in patients treated with placebo. The Cooperative Systematic Studies of Rheumatic Diseases Group. Arthritic Rheum. (1990) 33(4):477–484.
   PubMedGoogle Scholar