10.3929/ETHZ-B-000035831
Schaer, Corinne
Hiltbrunner, Stefanie
Ernst, Bettina
Mueller, Christoph
Kurrer, Michael
Kopf, Manfred
Harris, Nicola L.
HVEM Signalling Promotes Colitis
ETH Zurich
2011
Journal Article
2011-04-18
en
11 p.
application/pdf
Creative Commons Attribution 3.0 Unported
info:eu-repo/semantics/openAccess
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.
PLoS ONE, 6 (4)
ISSN:1932-6203