Harold L. Dickensheets

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Recently discovered type III IFNs (IFN-L) exert their antiviral and immunomodulatory activities through a unique receptor complex composed of IFN-LR1 and interleukin-10 receptor 2. To further study type III IFNs, we cloned and characterized mouse IFN-L ligand-receptor system. We showed that, similar to their human orthologues, mIFN-L2 and mIFN-L3 signal(More)
With the use of a partial sequence of the human genome, we identified a gene encoding a novel soluble receptor belonging to the class II cytokine receptor family. This gene is positioned on chromosome 6 in the vicinity of the IFNGR1 gene in a head-to-tail orientation. The gene consists of six exons and encodes a 231-aa protein with a 21-aa leader sequence.(More)
The primary interleukin-4 (IL-4) receptor complex on monocytes (type I IL-4 receptor) includes the 140-kDa alpha chain (IL-4R alpha) and the IL-2 receptor gamma chain, gamma(c), which heterodimerize for intracellular signaling, resulting in suppression of lipopolysaccharide (LPS)-inducible inflammatory mediator production. The activity of IL-13 on human(More)
The Th2-type cytokines, interleukin-4 (IL-4) and interleukin-13 (IL-13), induce expression of a distinct subset of genes in human monocytes, including FcepsilonRIIb (CD23), 15-lipoxygenase, IL-1 receptor antagonist (IL-1ra), and type I and type II IL-1 receptors (IL-1R). Type I interferons (IFN-alpha and IFN-beta) and type II interferon (IFN-gamma) inhibit(More)
2595 IL-4 and-13 are related cytokines, encoded by closely linked genes (1). IL-4 can signal through either the type I (IL-4R ␣ / ␥ c) or the type II (IL-4R ␣ /-13R ␣ 1) IL-4 receptor, whereas IL-13 signals exclusively via the type II IL-4 receptor (2). IL-4 binds to IL-4R ␣ with high affi nity, triggering receptor heterodimerization either with ␥ c or with(More)
TLR agonists such as LPS and poly(I:C) induce expression of type I IFNs, such as IFN-α and -β, by macrophages. To examine the role of IFN-β in the induction of ISGs by LPS, we compared the ability of LPS to induce ISGF3 activity and ISG expression in bone marrow-derived macrophages from WT and Ifnb1(-/-) mice. We found that LPS treatment activated ISGF3 and(More)
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