Pfeifer, Eva and Polz, Johannes and Griess, Sybille and Mostboeck, Sven and Hehlgans, Thomas and Maennel, Daniela N. (2012) Mechanisms of immune complex-mediated experimental glomerulonephritis: possible role of the balance between endogenous TNF and soluble TNF receptor type 2. EUROPEAN CYTOKINE NETWORK, 23 (1). pp. 15-20. ISSN 1148-5493,
Full text not available from this repository.Abstract
In an experimental model of immune-complex-mediated glomerulonephritis, mice excreted increased levels of urinary protein starting three days after the induction. Mice lacking the TNF receptor type 2 (TNFR2) were protected from early proteinuria and enhanced mortality. Analysis of the molecular basis of the mechanisms of glomerulonephritis revealed that naive mice continuously excrete soluble TNF-neutralizing TNFR2 in urine. Mice kept in a specific pathogen-free environment did not go on to develop early proteinuria or enhanced mortality, following induction of glomerulonephritis. TNFR2-deficient mice were protected from early proteinuria and enhanced mortality only when housed conventionally. Mice producing human TNFR2 that can be activated by mouse TNF, in addition to mouse TNFR2, did not demonstrate enhanced susceptibility to the lethal effects of glomerulonephritis, indicating that pro-inflammatory signalling via TNFR2 does not account for a sensitizing effect. Finally, we suggest that the protective effect seen in mice lacking TNFR2 results rather from environment-induced attenuation by low dose bacterial endotoxins than from missing pro-inflammatory signalling via the TNFR2.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TUMOR-NECROSIS-FACTOR; T-REGULATORY-CELLS; EXPRESSION; MOUSE; MICE; TOLERANCE; ENDOTOXIN; INJURY; ALPHA; tumor necrosis factor; p75TNF receptor; TNFR2; kidney; inflammation; tolerance |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Immunologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 18 May 2020 10:12 |
| Last Modified: | 18 May 2020 10:12 |
| URI: | https://pred.uni-regensburg.de/id/eprint/19082 |
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