Both Ab/SOD conjugates targeted to Plvap and CD31 accumulated in the lungs after IV injection in mice, but the former more profoundly inhibited LPS-induced pulmonary inflammation and elevation of plasma level of interferon-beta and -gamma and interleukin-27.
The lung inflammation of IL-27-deficient mice was characterized by more IFN-γ-producing CD8<sup>+</sup> T cells and fewer IL-10-producing CD8<sup>+</sup> T cells than that of wild-type mice.
Although signaling of IL-27/WSX-1 interactions have been recognized in the down-regulation of airway hyper-reactivity and in lung inflammation during the development of allergic asthma, little is known about the role of single nucleotide polymorphisms (SNPs) of IL-27 and individual susceptibility to asthma.