@Article{ecn.2012.0299,
AUTHOR = {Eva Pfeifer, Johannes Polz, Sybille Grieβl, Sven Mostböck, Thomas Hehlgans, Daniela N. Männel},
TITLE = {Mechanisms of immune complex-mediated experimental glomerulonephritis: possible role of the balance between endogenous TNF and soluble TNF receptor type 2},
JOURNAL = {European Cytokine Network},
VOLUME = {23},
YEAR = {2012},
NUMBER = {1},
PAGES = {15--20},
URL = {http://www.techscience.com/ECN/v23n1/65758},
ISSN = {1952-4005},
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 naïve 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.},
DOI = {10.1684/ecn.2012.0299}
}