Controlling Gut Inflammation by Restoring Anti-Inflammatory Pathways in Inflammatory Bowel Disease

Research output: Contribution to journalArticle

Abstract

Inflammatory bowel disease (IBD) is caused by a dysregulated immune response against normal components of the intestinal microflora combined with defective functioning of anti-inflammatory pathways. Currently, all therapies approved for IBD manipulate the immune system by inhibiting pro-inflammatory mechanisms, such as tumor necrosis factor-α, gut-homing α(4)β(7) integrin, interleukin-12/interleukin-23, and Janus kinases. However, some IBD patients are non-responders to these drugs, which are also associated with serious side effects. Thus, it has been hypothesized that therapies aimed at restoring anti-inflammatory signals, by exploiting the tolerogenic potential of cytokines (interleukin-10, transforming growth factor-β, granulocyte macrophage colony-stimulating factor), immune cells (regulatory T cells, tolerogenic dendritic cells), or mesenchymal stem cells, might offer promising results in terms of clinical efficacy with fewer side effects. In this review, we provide new insights into putative novel treatments aimed at restoring anti-inflammatory signaling pathways in IBD.
Original languageEnglish
JournalCells
Volume8
Issue number5
DOIs
Publication statusPublished - Apr 30 2019

Keywords

  • *Crohn’s disease
  • *granulocyte macrophage colony-stimulating factor
  • *interleukin-10
  • *mesenchymal stem cells
  • *regulatory T cells
  • *tolerogenic dendritic cells
  • *transforming growth factor-β
  • *ulcerative colitis
  • Anti-Inflammatory Agents/*therapeutic use
  • Cytokines/*antagonists & inhibitors
  • Dendritic Cells/*immunology
  • Humans
  • Immunotherapy
  • Inflammation/*therapy
  • Inflammatory Bowel Diseases/*therapy
  • Mesenchymal Stem Cells/*immunology
  • T-Lymphocytes, Regulatory/*immunology

Fingerprint Dive into the research topics of 'Controlling Gut Inflammation by Restoring Anti-Inflammatory Pathways in Inflammatory Bowel Disease'. Together they form a unique fingerprint.

  • Cite this