Article Text

PDF
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}mucosa.de

Statistics from Altmetric.com

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 …

View Full Text

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.