Download PDFPDF

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

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g.
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests


  • Responses are moderated before posting and publication is at the absolute discretion of BMJ, however they are not peer-reviewed
  • Once published, you will not have the right to remove or edit your response. Removal or editing of responses is at BMJ's absolute discretion
  • If patients could recognise themselves, or anyone else could recognise a patient from your description, please obtain the patient's written consent to publication and send them to the editorial office before submitting your response [Patient consent forms]
  • By submitting this response you are agreeing to our full [Response terms and requirements]

Vertical Tabs

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...

    Show More
    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...

    Show More
    Conflict of Interest:
    None declared.