HVEM signalling promotes colitis

Schaer, Corinne; Hiltbrunner, Stefanie; Ernst, Bettina; Mueller, Christoph; Kurrer, Michael; Kopf, Manfred; Harris, Nicola L (2011). HVEM signalling promotes colitis. PLoS ONE, 6(4), e18495. Lawrence, Kans.: Public Library of Science 10.1371/journal.pone.0018495

[img]
Preview
Text
journal.pone.0018495.pdf - Published Version
Available under License Creative Commons: Attribution (CC-BY).

Download (1MB) | Preview

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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Service Sector > Institute of Pathology

UniBE Contributor:

Müller, Christoph

ISSN:

1932-6203

Publisher:

Public Library of Science

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 14:18

Last Modified:

28 Dec 2014 09:11

Publisher DOI:

10.1371/journal.pone.0018495

PubMed ID:

21533159

Web of Science ID:

000289620100007

BORIS DOI:

10.7892/boris.5527

URI:

https://boris.unibe.ch/id/eprint/5527 (FactScience: 210280)

Actions (login required)

Edit item Edit item
Provide Feedback