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Indeed, iv treatment with FvEjw siRNA complexed with RVG-9R was able to protect mice from fatal JEV-induced encephalitis.
Intravenous treatment with siFvE + RVG-9R was also able to protect 80% of inoculated mice from fatal flaviviral encephalitis.
Most recently, passive immunization with α-hemolysin-neutralizing antibodies has been shown to protect mice from fatal S. aureus pneumonia [12], [13].
Both rhAbs gave 50% neutralization of H5N1 viruses in the 0.2 12.5 µg/ml range and protected 100% of mice from fatal disease at a dose of 2.5 mg/kg, doses that were comparable to the virus-neutralizing and lowest in vivo protective concentrations of human H5-specific mAbs derived from memory B cells of a clade 1 H5N1 virus-infected patients reported elsewhere [21].
Lip40 also protected 75%% of mice from fatal virulent A. pleuropneumoniae infection.
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The importance of FVII activity for the perinatal coagulation status and morbidity is further demonstrated in f7-/ mice who suffer from fatal perinatal bleeding: 70% of them have fatal intra-abdominal bleeding within the first day of life, whereas most of the remaining neonates die from intracranial hemorrhage before the age of 24 days [ 20].
The model to assess suppressor activity in vivo was to protect mice from a rapidly fatal GVHD as described previously[36].
The addition of human CD4+ cells primed with IL-2 and TGF-β (T-TGF-β) also could not protect mice from this rapidly fatal xeno-GVHD.
The methodology used to prepare human iTregs in this study resulted in suppressive activity that was equivalent to that of nTregs in protecting immunodeficient mice from a rapidly fatal xeno-GVHD.
Similarly in vivo, delivering T-oligos intravenously twice daily for two periods of five days each appears to rescue some mice from otherwise rapidly fatal innocula of tumor cells and to significantly increase survival overall.
Consequently, Irf4 /– mice established chronic infections, but were protected from fatal immunopathology.
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