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Soluble tumor necrosis factor receptor improves autoimmune neuritis in mice.
2003 MAY 7 - (NewsRx.com & NewsRx.net) -- Exogenous soluble tumor necrosis factor receptor type I improved murine experimental autoimmune neuritis.
According to a study from Sweden, "Tumor necrosis factor (TNF) and its receptor (TNFR) have been strongly implicated in the pathogenesis of autoimmune disease. Soluble cytokine receptors may be shed naturally from cell membranes to inhibit cytokine activity. Experimental autoimmune neuritis (EAN) is a CD4 Th1 cell-mediated animal model of Guillain-Barre syndrome (GBS) in humans."
"In the present study, we investigated the effects of soluble TNFR type I (sTNFR I) in EAN induced in mice by PO peptide 180-199 and Freund's complete adjuvant," reported Lei Bao and collaborators at the Karolinska Institutet in Stockholm. "Our data from two different therapeutic regimens indicate that the administration of sTNFR I effectively ameliorated the clinical and pathological signs of EAN, i.e., decreased its severity, shortened its duration, and reduced inflammatory cell infiltration into the peripheral nervous system. The suppression of clinical EAN was accompanied in vitro by a marked reduction in antigen-specific ...
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Source: HighBeam Research, Soluble tumor necrosis factor receptor improves autoimmune neuritis...