Dayer Schneider, Johanna; Seibold, Inge; Saxer-Sekulic, Nikolina; Paredes, Bruno E; Saurer, Leslie; Mueller, Christoph (2009). Lack of TNFR2 expression by CD4(+) T cells exacerbates experimental colitis. European journal of immunology, 39(7), pp. 1743-53. Weinheim: Wiley-VCH 10.1002/eji.200839132
Full text not available from this repository.TNF plays fundamental roles in the induction and perpetuation of inflammation. The effects of TNF are mediated through TNF receptor (TNFR) 1 or 2. As these two receptors mediate different functions, selective targeting of one receptor may represent a more specific treatment for inflammatory disorders than the complete blocking of TNF. TNFR2 expression is up-regulated in inflammatory bowel disease. Hence, we directly assessed the role of TNFR2 signaling in the CD4(+) T-cell transfer model of colitis using TNFR2(-/-) or WT mice as donors of colitogenic CD4(+)CD45RB(hi) T cells for transfer into syngeneic RAG2(-/-) or RAG2(-/-)TNFR2(-/-) recipient mice. Although the absence of TNFR2 expression by non-lymphoid cells of the recipient mice does not influence the course of colitis, transfer of TNFR2(-/-) CD4(+) T cells leads to an accelerated onset of disease and to more severe signs of inflammation. The enhanced colitogenic potential of TNFR2(-/-) CD4(+) T cells is associated with reduced activation-induced cell death, resulting in an increased accumulation of TNFR2(-/-) CD4(+) T cells. Hence, TNFR2 signaling is crucial for the TNF-dependent contraction of the disease-inducing T cells. Therefore, a selective blocking of TNFR2 may lead to exacerbation rather than attenuation of T-cell-mediated inflammatory disorders.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Service Sector > Institute of Pathology |
UniBE Contributor: |
Saurer, Leslie, Müller, Christoph (C) |
ISSN: |
0014-2980 |
ISBN: |
19551899 |
Publisher: |
Wiley-VCH |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:08 |
Last Modified: |
29 Mar 2023 23:33 |
Publisher DOI: |
10.1002/eji.200839132 |
PubMed ID: |
19551899 |
Web of Science ID: |
000268270900007 |
URI: |
https://boris.unibe.ch/id/eprint/30009 (FactScience: 165719) |
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