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Interleukin-12 (IL-12), IL-23 and interferon-γ (IFN-γ) are pivotal cytokines acting in concert with tumor necrosis factor (TNF) and IL-1β to shape type I immune responses against bacterial pathogens. Recently, several groups reported that type I immunity can be inhibited by IFN-α/β. Here we show the extent of the inhibitory effects of IFN-α and IFN-β on the responsiveness of human monocytes to Toll...
Glucocorticoids acting through the glucocorticoid receptor (GR) inhibit TNF-induced lethal inflammation. We demonstrate the increased TNF sensitivity of mice expressing a mutant GR (GR dim/dim ), which does not dimerize or induce GRE genes. Induction of MKP-1 seems essential for GR control of TNF-induced inflammation: TNF fails to induce the MKP-1-encoding gene Dusp1 in GR dim/dim ...
To determine to what extent lipopolysaccharide-induced IL-10 production capacity is determined by polymorphisms in toll-like receptor-4 (TLR4) and the IL-10 promoter region, we measured in vivo IL-10 and TNF-α production in patients undergoing elective cardiopulmonary bypass surgery, a major surgical trauma associated with ischemia-reperfusion injury that triggers an endotoxemia and profound inflammatory...
Humans exhibit substantial inter-individual differences in TNF-α production upon endotoxin stimulation. To determine to what extent the lipopolysaccharide-induced TNF-α production capacity in vivo and ex vivo is determined by polymorphisms in toll-like receptor-4 (TLR4), the TNF-α promoter region and Nod2, we screened for two TLR4 polymorphisms, a Nod2 polymorphism and the TNF-α promoter polymorphisms...
Studies of mice with a targeted disruption of the CCR5 gene suggest that the CC chemokine receptor 5 (CCR5) is a determinant of the cytokine response to endotoxin. In humans, a naturally occurring mutation of the CCR5 gene is a 32-basepair (bp) deletion which precludes the translation of the gene into a functional transmembrane protein. To evaluate the cytokine phenotype of heterozygosity for the...
Tumour necrosis factor (TNF) is a key regulator of inflammation and immunity. The cellular effects exerted by TNF depend, apart from NF-κB-directed gene transcription, largely on its ability to activate phospholipase A 2 (PLA 2 ), yielding the release of arachidonic acid (AA) and its metabolites. AA metabolites, especially the leukotrienes, act as second messengers in TNF receptor...
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