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A possible link between TIMP-1 induction and response to infliximab
  1. S Derer1,
  2. G H Waetzig2,
  3. D Seegert2,
  4. S Nikolaus3,
  5. S Schreiber1,3,
  6. P Rosenstiel1
  1. 1
    Institute of Clinical Molecular Biology, University Hospital Schleswig-Holstein, Kiel, Germany
  2. 2
    CONARIS Research Institute AG, Kiel, Germany
  3. 3
    Department of General Internal Medicine, University Hospital Schleswig-Holstein, Kiel, Germany
  1. Dr P Rosenstiel, Institute of Clinical Molecular Biology, University Hospital Schleswig-Holstein, Campus Kiel, Schittenhelmstrasse 12, D-24105 Kiel, Germany; p.rosenstiel{at}

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In their recent study, Van den Brande and colleagues (Gut 2007;56:509–17) demonstrated the induction of apoptosis by infliximab in lamina propria T lymphocytes of patients with Crohn’s disease (CD) in situ and showed a correlation between 99mTc-annexin V uptake and and response to infliximab treatment. Interestingly, Nesbitt et al1 reported that the novel antitumour necrosis factor (TNF) compound certolizumab pegol does not induce apoptosis despite its clinical activity. A recent paper by Di Sabatino and colleagues2 reports that the production of tissue inhibitor of metalloproteinases (TIMP)-1 is enhanced in myofibroblasts from patients with CD by infliximab in a mitogen-activated protein kinase (MAPK) p38-dependent manner. This effect was not accompanied by significant induction of …

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  • Competing interests: None.

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