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Defective mucosal T cell death is sustainably reverted by infliximab in a caspase dependent pathway in Crohn’s disease
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Other responses

  • Published on:
    Re: Modulation of p38MAPK and STAT3 signalling by infliximab and etanercept in intestinal T-cells
    • Antonio Di Sabatino, MD
    • Other Contributors:
      • Rachele Ciccocioppo, Raffaele Morera, and Gino R. Corazza

    Dear Editor

    We thank Rosenstiel et al for their interest in our paper regarding the role of the chimeric anti-tumor necrosis factor (TNF)-alpha antibody, infliximab, in reverting defective lamina propria T-cell apoptosis in Crohn’s disease via a caspase-dependent pathway.[1]

    In their interesting letter Rosenstiel et al investigate the complex TNF-alpha blocker machinery in Crohn’s disease...

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    Conflict of Interest:
    None declared.
  • Published on:
    Modulation of p38MAPK and STAT3 signalling by infliximab and etanercept in intestinal T-cells
    • Philip Rosenstiel, MD
    • Other Contributors:
      • Jorgen Agnholt, Jens Kelsen, Valentina Medici, Georg H. Waetzig, Dirk Seegert and Stefan Schreiber

    Dear Editor

    There is growing evidence that the efficacy of anti-TNF-a therapies in Crohn’s disease (CD) may critically depend on the binding of the transmembrane precursor of TNF-a (mTNF-a), thus eliciting complex intracellular signaling events, a process described as ‘reverse signaling’.[1-3]

    In their recent paper, Di Sabatino et al.[4] have shown that infliximab reverts defective peripheral and la...

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    Conflict of Interest:
    None declared.