HVEM signalling promotes colitis

PLoS One. 2011 Apr 18;6(4):e18495. doi: 10.1371/journal.pone.0018495.


Background: Tumor necrosis factor super family (TNFSF) members regulate important processes involved in cell proliferation, survival and differentiation and are therefore crucial for the balance between homeostasis and inflammatory responses. Several members of the TNFSF are closely associated with inflammatory bowel disease (IBD). Thus, they represent interesting new targets for therapeutic treatment of IBD.

Methodology/principal findings: We have used mice deficient in TNFSF member HVEM in experimental models of IBD to investigate its role in the disease process. Two models of IBD were employed: i) chemical-induced colitis primarily mediated by innate immune cells; and ii) colitis initiated by CD4(+)CD45RB(high) T cells following their transfer into immuno-deficient RAG1(-/-) hosts. In both models of disease the absence of HVEM resulted in a significant reduction in colitis and inflammatory cytokine production.

Conclusions: These data show that HVEM stimulatory signals promote experimental colitis driven by innate or adaptive immune cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Base Sequence
  • CD4-Positive T-Lymphocytes / immunology
  • Colitis / metabolism*
  • DNA Primers
  • Flow Cytometry
  • Mice
  • Mice, Inbred C57BL
  • Receptors, Tumor Necrosis Factor, Member 14 / genetics
  • Receptors, Tumor Necrosis Factor, Member 14 / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction*


  • DNA Primers
  • Receptors, Tumor Necrosis Factor, Member 14
  • Tnfrsf14 protein, mouse