id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-310444-02dsqbeg	Mahlakoiv, T.	P136 Combined action of type I and type III IFN restricts initial replication of SARS-coronavirus in the lung but fails to inhibit systemic virus spread	2012-09-30		.txt	text/plain	2273	127	47	Conclusion Our data suggest that the failure of STAT1-deficient mice to efficiently control initial SARS-CoV replication in the lung is due to impaired type I and type III IFN signaling, whereas the failure to control subsequent systemic viral spread is due to unrelated defects in STAT1-deficient mice. The type III interferons are especially important in pulmonary infection, produced in response to viral infection and bacterial PAMPs. IFN-k is activated by and induces NF-jB signaling and promotes expression of Th1 cytokines. Consistent with the expected participation of IFN-k in NF-jB signaling, we measured decreased expression of KC, TNF and GM-CSF and increased IL-10 in the IL-28RÀ/ -BAL (P < 0.05), although there were no significant differences in the populations of immune cells (neutrophils, DC, macrophages) recruited to the airways of the wild type or IL-28RÀ/À mice. Ligation of immunoreceptor tyrosine-based activation motif (ITAM)associated receptors in macrophages can initiate potent induction of negative regulators, including anti-inflammatory cytokine IL-10, signaling inhibitors SOCS3, ABIN3, A20 and transcriptional repressor Hes1 [1] .	./cache/cord-310444-02dsqbeg.txt	./txt/cord-310444-02dsqbeg.txt