457
Views
38
CrossRef citations to date
0
Altmetric
Review

Mode of function of biological anti-TNF agents in the treatment of inflammatory bowel diseases

, MD, &
Pages 1051-1059 | Published online: 31 Jul 2007

Bibliography

  • PODOLSKY DK: Inflammatory bowel disease. N. Engl. J. Med. (2002) 347(6):417-429.
  • TRAVIS SP, STANGE EF, LEMANN M et al.: European evidence based consensus on the diagnosis and management of Crohn's disease: current management. Gut (2006) 55(Suppl. 1):i16-i35.
  • HANAUER SB: Medical therapy for ulcerative colitis 2004. Gastroenterology (2004) 126(6):1582-1592.
  • WARE CF: Network communications: lymphotoxins, LIGHT, and TNF. Ann. Rev. Immunol. (2005) 23:787-819.
  • PAPADAKIS KA, TARGAN SR: Tumor necrosis factor: biology and therapeutic inhibitors. Gastroenterology (2000) 119(4):1148-1157.
  • SARTOR RB: Mechanisms of disease: pathogenesis of Crohn's disease and ulcerative colitis. Nat. Clin. Pract. Gastroenterol. Hepatol. (2006) 3(7):390-407.
  • CHANG JT, LICHTENSTEIN GR: Drug insight: antagonists of TNF-α in the treatment of inflammatory bowel disease. Nat. Clin. Pract. Gastroenterol. Hepatol. (2006) 3(4):220-228.
  • BRAEGGER CP, NICHOLLS S, MURCH SH, STEPHENS S, MACDONALD TT: TNF-α in stool as a marker of intestinal inflammation. Lancet (1992) 339(8785):89-91.
  • MURCH SH, BRAEGGER CP, WALKER-SMITH JA, MACDONALD TT: Location of TNF-α by immunohistochemistry in chronic inflammatory bowel disease. Gut (1993) 34(12):1705-1709.
  • BAMIAS G, NYCE MR, DE LA RUE SA, COMINELLI F: New concepts in the pathophysiology of inflammatory bowel disease. Ann. Intern. Med. (2005) 143(12):895-904.
  • HELLER F, FUSS IJ, NIEUWENHUIS EE, BLUMBERG RS, STROBER W: Oxazolone colitis, a TH2 colitis model resembling ulcerative colitis, is mediated by IL-13-producing NK-T cells. Immunity (2002) 17(5):629-638.
  • HELLER F, FLORIAN P, BOJARSKI C et al.: Interleukin-13 is the key effector TH2 cytokine in ulcerative colitis that affects epithelial tight junctions, apoptosis, and cell restitution. Gastroenterology (2005) 129(2):550-564.
  • BOUMA G, STROBER W: The immunological and genetic basis of inflammatory bowel disease. Nat. Rev. Immunol. (2003) 3(7):521-533.
  • STROBER W, KELSALL B, FUSS I et al.: Reciprocal IFN-γ and TGF-β responses regulate the occurrence of mucosal inflammation. Immunol. Today (1997) 18(2):61-64.
  • CORAZZA N, BRUNNER T, BURI C et al.: Transmembrane tumor necrosis factor is a potent inducer of colitis even in the absence of its secreted form. Gastroenterology (2004) 127(3):816-825.
  • NAKAI M, SUDO K, YAMADA Y et al.: The role of the tumor necrosis factor receptor in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Dig. Dis. Sci. (2005) 50(9):1669-1676.
  • SHEN C, DE HERTOGH G, BULLENS DM et al.: Remission-inducing effect of anti-TNF monoclonal antibody in TNBS colitis: mechanisms beyond neutralization? Inflamm. Bowel Dis. (2007) 13(3):308-316.
  • TE VELDE AA, DE KORT F, STERRENBURG E et al.: Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease. Inflamm. Bowel Dis. (2007) 13(3):325-330.
  • TARGAN SR, HANAUER SB, VAN DEVENTER SJ et al.: A short-term study of chimeric monoclonal antibody cA2 to TNF-α for Crohn's disease. Crohn's Disease cA2 Study Group. N. Engl. J. Med. (1997) 337(15):1029-1035.
  • PRESENT DH, RUTGEERTS P, TARGAN S et al.: Infliximab for the treatment of fistulas in patients with Crohn's disease. N. Engl. J. Med. (1999) 340(18):1398-1405.
  • HANAUER SB, FEAGAN BG, LICHTENSTEIN GR et al.: Maintenance infliximab for Crohn's disease: the ACCENT I randomised trial. Lancet (2002) 359(9317):1541-1549.
  • SANDS BE, ANDERSON FH, BERNSTEIN CN et al.: Infliximab maintenance therapy for fistulizing Crohn's disease. N. Engl. J. Med. (2004) 350(9):876-885.
  • RUTGEERTS P, SANDBORN WJ, FEAGAN BG et al.: Infliximab for induction and maintenance therapy for ulcerative colitis. N. Engl. J. Med. (2005) 353(23):2462-2476.
  • HANAUER SB, SANDBORN WJ, RUTGEERTS P et al.: Human anti-TNF monoclonal antibody (adalimumab) in Crohn's disease: the CLASSIC-I trial. Gastroenterology (2006) 130(2):323-333.
  • SCHREIBER S, RUTGEERTS P, FEDORAK RN et al.: A randomized, placebo-controlled trial of certolizumab pegol (CDP870) for treatment of Crohn's disease. Gastroenterology (2005) 129(3):807-818.
  • SHEN C, MAERTEN P, GEBOES K, VAN ASSCHE G, RUTGEERTS P, CEUPPENS JL: Infliximab induces apoptosis of monocytes and T lymphocytes in a human-mouse chimeric model. Clin. Immunol. (2005) 115(3):250-259.
  • WAETZIG GH, ROSENSTIEL P, ARLT A et al.: Soluble tumor necrosis factor (TNF) receptor-1 induces apoptosis via reverse TNF signaling and autocrine transforming growth factor-β1. FASEB J. (2005) 19(1):91-93.
  • LUGERING A, SCHMIDT M, LUGERING N, PAUELS HG, DOMSCHKE W, KUCHARZIK T: Infliximab induces apoptosis in monocytes from patients with chronic active Crohn's disease by using a caspase-dependent pathway. Gastroenterology (2001) 121(5):1145-1157.
  • TEN HOVE T, VAN MONTFRANS C, PEPPELENBOSCH MP, VAN DEVENTER SJ: Infliximab treatment induces apoptosis of lamina propria T lymphocytes in Crohn's disease. Gut (2002) 50(2):206-211.
  • ARNOLD R, BRENNER D, BECKER M, FREY CR, KRAMMER PH: How T lymphocytes switch between life and death. Eur. J. Immunol. (2006) 36(7):1654-1658.
  • VAN DEN BRANDE JM, BRAAT H, VAN DEN BRINK GR et al.: Infliximab but not etanercept induces apoptosis in lamina propria T-lymphocytes from patients with Crohn's disease. Gastroenterology (2003) 124(7):1774-1785.
  • SHEN C, ASSCHE GV, COLPAERT S et al.: Adalimumab induces apoptosis of human monocytes: a comparative study with infliximab and etanercept. Aliment. Pharmacol. Ther. (2005) 21(3):251-258.
  • VAN DEN BRANDE JM, KOEHLER T, ZELINKOVA Z et al.: Prediction of anti-TNF clinical efficacy by real-time visualisation of apoptosis in patients with Crohn's disease. Gut (2007) 56(4):509-517.
  • FOSSATI G, NESBITT A: Effect of the anti-TNF agents, adalimumab, etanercept, infliximab, and certolizumab PEGOL (CDP870) on the induction of apoptosis in activated peripheral blood lymphocytes and monocytes. Am. J. Gastroenterol. (2005) 100(Suppl.):299.
  • LUDWICZEK O, KASER A, TILG H: Plasma levels of soluble CD40 ligand are elevated in inflammatory bowel diseases. Int. J. Colorectal Dis. (2003) 18(2):142-147.
  • GRAF D, KORTHAUER U, MAGES HW, SENGER G, KROCZEK RA: Cloning of TRAP, a ligand for CD40 on human T cells. Eur. J. Immunol. (1992) 22(12):3191-3194.
  • DANESE S, SANS M, SCALDAFERRI F et al.: TNF-α blockade down-regulates the CD40/CD40L pathway in the mucosal microcirculation: a novel anti-inflammatory mechanism of infliximab in Crohn's disease. J. Immunol. (2006) 176(4):2617-2624.
  • MITOMA H, HORIUCHI T, HATTA N et al.: Infliximab induces potent anti-inflammatory responses by outside-to-inside signals through transmembrane TNF-α. Gastroenterology (2005) 128(2):376-392.
  • EHRENSTEIN MR, EVANS JG, SINGH A et al.: Compromised function of regulatory T cells in rheumatoid arthritis and reversal by anti-TNF-α therapy. J. Exp. Med. (2004) 200(3):277-285.
  • NADKARNI S, MAURI C, EHRENSTEIN MR: Anti-TNF-{α} therapy induces a distinct regulatory T cell population in patients with rheumatoid arthritis via TGF-{β}. J. Exp. Med. (2007) 204:33-39.
  • ROSENSTIEL P, AGNHOLT J, KELSEN J et al.: Differential modulation of p38 mitogen activated protein kinase and STAT3 signalling pathways by infliximab and etanercept in intestinal T cells from patients with Crohn's disease. Gut (2005) 54(2):314-315.
  • WAETZIG GH, SEEGERT D, ROSENSTIEL P, NIKOLAUS S, SCHREIBER S: p38 mitogen-activated protein kinase is activated and linked to TNF-α signaling in inflammatory bowel disease. J. Immunol. (2002) 168(10):5342-5351.
  • WAETZIG GH, ROSENSTIEL P, NIKOLAUS S, SEEGERT D, SCHREIBER S: Differential p38 mitogen-activated protein kinase target phosphorylation in responders and nonresponders to infliximab. Gastroenterology (2003) 125(2):633-634.
  • AGNHOLT J, KALTOFT K: Infliximab downregulates interferon-γ production in activated gut T-lymphocytes from patients with Crohn's disease. Cytokine (2001) 15(4):212-222.
  • VERMEIRE S, VAN ASSCHE G, RUTGEERTS P: The role of C-reactive protein as an inflammatory marker in gastrointestinal diseases. Nat. Clin. Pract. Gastroenterol. Hepatol. (2005) 2(12):580-586.
  • VERMEIRE S, VAN ASSCHE G, RUTGEERTS P: Laboratory markers in IBD: useful, magic, or unnecessary toys? Gut (2006) 55(3):426-431.
  • FAMILIAN A, VOSKUYL AE, VAN MIERLO GJ et al.: Infliximab treatment reduces complement activation in patients with rheumatoid arthritis. Ann. Rheum. Dis. (2005) 64(7):1003-1008.
  • ARNOTT ID, SHAND A, GHOSH S: Administration of infliximab in Crohn's disease does not deplete complement components C3 and C4. Am. J. Gastroenterol. (2000) 95(11):3326-3327.
  • ZIMMERMANN-NIELSEN E, AGNHOLT J, THORLACIUS-USSING O, DAHLERUP JF, BAATRUP G: Complement activation in plasma before and after infliximab treatment in Crohn disease. Scand. J. Gastroenterol. (2003) 38(10):1050-1054.
  • CANETE JD, PABLOS JL, SANMARTI R et al.: Antiangiogenic effects of anti-TNF-α therapy with infliximab in psoriatic arthritis. Arthritis Rheum. (2004) 50(5):1636-1641.
  • LOUIS E, VERMEIRE S, RUTGEERTS P et al.: A positive response to infliximab in Crohn disease: association with a higher systemic inflammation before treatment but not with -308 TNF gene polymorphism. Scand. J. Gastroenterol. (2002) 37(7):818-824.
  • SCHREIBER S: Adalimumab induces and maintains clinical remission independent of baseline CRP concentration in Crohn's disease: subanalysis of the CHARM study. Gut (2006) 38(Suppl. 2):A21.
  • WILLOT S, VERMEIRE S, OHRESSER M et al.: No association between C-reactive protein gene polymorphisms and decrease of C-reactive protein serum concentration after infliximab treatment in Crohn's disease. Pharmacogenet. Genomics (2006) 16(1):37-42.
  • MINDERHOUD IM, OLDENBURG B, WISMEIJER JA, BERGE HENEGOUWEN GP, SMOUT AJ: IBS-like symptoms in patients with inflammatory bowel disease in remission; relationships with quality of life and coping behavior. Dig. Dis. Sci. (2004) 49(3):469-474.
  • VERMEIRE S, LOUIS E, CARBONEZ A et al.: Demographic and clinical parameters influencing the short-term outcome of anti-TNF (infliximab) treatment in Crohn's disease. Am. J. Gastroenterol. (2002) 97(9):2357-2363.
  • FEFFERMAN DS, LODHAVIA PJ, ALSAHLI M et al.: Smoking and immunomodulators do not influence the response or duration of response to infliximab in Crohn's disease. Inflamm. Bowel Dis. (2004) 10(4):346-351.
  • ORLANDO A, COLOMBO E, KOHN A et al.: Infliximab in the treatment of Crohn's disease: predictors of response in an Italian multicentric open study. Dig. Liver Dis. (2005) 37(8):577-583.
  • PARSI MA, ACHKAR JP, RICHARDSON S et al.: Predictors of response to infliximab in patients with Crohn's disease. Gastroenterology (2002) 123(3):707-713.
  • LAMIREAU T, CEZARD JP, DABADIE A et al.: Efficacy and tolerance of infliximab in children and adolescents with Crohn's disease. Inflamm. Bowel Dis. (2004) 10(6):745-750.
  • MARKOWITZ J, HYAMS J, MACK D et al.: Corticosteroid therapy in the age of infliximab: acute and 1-year outcomes in newly diagnosed children with Crohn's disease. Clin. Gastroenterol. Hepatol. (2006) 4(9):1124-1129.
  • LAHARIE D, SALZMANN M, BOUBEKEUR H et al.: Predictors of response to infliximab in luminal Crohn's disease. Gastroenterol. Clin. Biol. (2005) 29(2):145-149.
  • HLAVATY T, PIERIK M, HENCKAERTS L et al.: Polymorphisms in apoptosis genes predict response to infliximab therapy in luminal and fistulizing Crohn's disease. Aliment. Pharmacol. Ther. (2005) 22(7):613-626.
  • HLAVATY T, FERRANTE M, HENCKAERTS L, PIERIK M, RUTGEERTS P, VERMEIRE S: Predictive model for the outcome of infliximab therapy in Crohn's disease based on apoptotic pharmacogenetic index and clinical predictors. Inflamm. Bowel Dis. (2006).
  • MASCHERETTI S, SCHREIBER S: Genetic testing in Crohn disease: utility in individualizing patient management. Am. J. Pharmacogenomics (2005) 5(4):213-222.
  • MASCHERETTI S, HAMPE J, CROUCHER PJ et al.: Response to infliximab treatment in Crohn's disease is not associated with mutations in the CARD15 (NOD2) gene: an analysis in 534 patients from two multicenter, prospective GCP-level trials. Pharmacogenetics (2002) 12(7):509-515.
  • DIDEBERG V, LOUIS E, FARNIR F et al.: Lymphotoxin α gene in Crohn's disease patients: absence of implication in the response to infliximab in a large cohort study. Pharmacogenet. Genomics (2006) 16(5):369-373.
  • VERMEIRE S, NOMAN M, VAN ASSCHE G, BAERT F, D'HAENS G, RUTGEERTS PJ: The effectiviness of concomitant immunosuppressive therapy to suppress formation of antibodies to infliximab in Crohn's disease. Gut (2007).
  • KEANE J, GERSHON S, WISE RP et al.: Tuberculosis associated with infliximab, a TNF-α-neutralizing agent. N. Engl. J. Med. (2001) 345(15):1098-1104.
  • TAI TL, O'ROURKE KP, MCWEENEY M, BURKE CM, SHEEHAN K, BARRY M: Pneumocystis carinii pneumonia following a second infusion of infliximab. Rheumatology (Oxford) (2002) 41(8):951-952.
  • MACKEY AC, GREEN L, LIANG LC, DINNDORF P, AVIGAN M: Hepatosplenic T cell lymphoma associated with infliximab use in young patients treated for inflammatory bowel disease. J. Pediatr. Gastroenterol. Nutr. (2007) 44(2):265-267.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.