HVEM signalling promotes colitis

Corinne Schaer, Stefanie Hiltbrunner, Bettina Ernst, Christoph Mueller, Michael Kurrer, Manfred Kopf, Nicola L. Harris

Research output: Contribution to journalArticleResearchpeer-review

12 Citations (Scopus)

Abstract

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+CD45RBhigh 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.

Original languageEnglish
Article numbere18495
Number of pages11
JournalPLoS ONE
Volume6
Issue number4
DOIs
Publication statusPublished - 29 Apr 2011
Externally publishedYes

Cite this