HVEM signalling promotes colitis.

HVEM signalling promotes colitis.

<h4>Background</h4>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 close...

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Autores principales: Corinne Schaer, Stefanie Hiltbrunner, Bettina Ernst, Christoph Mueller, Michael Kurrer, Manfred Kopf, Nicola L Harris
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Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2011
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Acceso en línea:https://doaj.org/article/42a907679a3b4ea18df5a1df17e8fc85
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spelling oai:doaj.org-article:42a907679a3b4ea18df5a1df17e8fc852021-11-18T06:55:37ZHVEM signalling promotes colitis.1932-620310.1371/journal.pone.0018495https://doaj.org/article/42a907679a3b4ea18df5a1df17e8fc852011-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21533159/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>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.<h4>Methodology/principal findings</h4>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.<h4>Conclusions</h4>These data show that HVEM stimulatory signals promote experimental colitis driven by innate or adaptive immune cells.Corinne SchaerStefanie HiltbrunnerBettina ErnstChristoph MuellerMichael KurrerManfred KopfNicola L HarrisPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 4, p e18495 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Corinne Schaer
Stefanie Hiltbrunner
Bettina Ernst
Christoph Mueller
Michael Kurrer
Manfred Kopf
Nicola L Harris
HVEM signalling promotes colitis.
description <h4>Background</h4>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.<h4>Methodology/principal findings</h4>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.<h4>Conclusions</h4>These data show that HVEM stimulatory signals promote experimental colitis driven by innate or adaptive immune cells.
format article
author Corinne Schaer
Stefanie Hiltbrunner
Bettina Ernst
Christoph Mueller
Michael Kurrer
Manfred Kopf
Nicola L Harris
author_facet Corinne Schaer
Stefanie Hiltbrunner
Bettina Ernst
Christoph Mueller
Michael Kurrer
Manfred Kopf
Nicola L Harris
author_sort Corinne Schaer
title HVEM signalling promotes colitis.
title_short HVEM signalling promotes colitis.
title_full HVEM signalling promotes colitis.
title_fullStr HVEM signalling promotes colitis.
title_full_unstemmed HVEM signalling promotes colitis.
title_sort hvem signalling promotes colitis.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/42a907679a3b4ea18df5a1df17e8fc85
work_keys_str_mv AT corinneschaer hvemsignallingpromotescolitis
AT stefaniehiltbrunner hvemsignallingpromotescolitis
AT bettinaernst hvemsignallingpromotescolitis
AT christophmueller hvemsignallingpromotescolitis
AT michaelkurrer hvemsignallingpromotescolitis
AT manfredkopf hvemsignallingpromotescolitis
AT nicolalharris hvemsignallingpromotescolitis
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