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IL-27 production was elevated during Clostridium difficile infection in humans and mice. Infected WSX-1-/- mice experienced increased weight loss, enhanced colonic histology damage, less Clostridium difficile clearance, and decreased survival compared to wild-type controls during Clostridium difficile infection.
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this paper shows that the increased protection and pathology in Mycobacterium tuberculosis-infected IL-27R-alpha-deficient mice is supported by IL-17A and is associated with the IL-17A-induced expansion of multifunctional T cells
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show that IL-27R signaling controls endothelial cells activation and myeloid cell recruitment at early and advanced stages of atherosclerosis. In the absence of IL-27R myeloid cells become hyperactivated, produce pro-inflammatory cytokines and act as more potent antigen presenting cells.
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data suggested that IL-27/IL-27R expression induced by Toxoplasma gondii infection may regulate mast cell-mediated immune response during acute ocular toxoplasmosis in mouse model
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Study reports a high-incidence, low-variation spontaneous mouse model of spondyloarthropathy that delineates how the combination of inflammatory cytokine interleukin-27 (IL-27) signaling deficiency and mitogenic signaling (mutant p53R172H) in vivo, leads to bone loss in the vertebral bodies and ossification of the cartilage in the intervertebral discs.
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IL-27 signaling in Foxp3(+) Tregs essential for Tregs to control autoimmune inflammation in the central nervous system
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The combination of mutant p53 & IL27RA(-/-) causes spontaneous liver inflammation, steatosis, and fibrosis, whereas either gene alone has no effects on the liver.
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IL-10 production by CD4(+) YFP(+) T cells is controlled systemically during malaria infection through IL-27 receptor signaling that is supported after CD4(+) T cell priming by ICOS signaling.
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The significant expression of IL-27 in TB and the negative influence of IL-27R on T cell function demonstrate the pathway by which this cytokine/receptor pair is detrimental in TB.
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IL-27R-mediated regulation of IL-17 controls the development of respiratory syncytial virus-associated pathogenesis.
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CCL4 and CCL5 expression was higher in livers of infected WSX-1(-/-) mice than infected WT mice, and hepatic CD4 T cells from WSX-1(-/-) mice expressed higher levels of CCR5 than cells from WT mice
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The loss of IL-27R signaling across the whole mouse resulted in reduced viral control and a slight increase in the number of virus-specific CD4 T cells at early stages of viral infection.
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Diminution of the Th1 response in infected Il27ra mice in vivo by neutralization of IL-12p40 attenuated CCR5 expression.
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These findings establish a novel antiatherogenic role for IL-27 receptor signaling, which acts to suppress the production of proinflammatory cytokines and chemokines and to curb the recruitment of inflammatory myeloid cells into atherosclerotic aortas.
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In Th1-dependent autoinflammatory lesions, IL-27Ralpha has a biphasic role in vivo, initially pathogenic, but ultimately playing a protective role by regulating immune responses and attenuating disease.
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Data show that the deletion of Il27ra ameliorates pathology in the pristane-induced SLE model.
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Findings demonstrate the essential role of IL-27R signaling in regulating effector T cell function during malaria infection and reveal a novel pathway that might be amenable to manipulation by drugs or vaccines.
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A novel role is revealed for WSX-1 as an inhibitory regulator of cytokine production and inflammation in Con A-induced hepatitis.
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The requirement for WSX-1 signaling in T helper type 1 cell differentiation is restricted to conditions in which IL-4 is produced.
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demonstrate an important role for WSX-1 signaling in the promotion of type 1 responses and chronic gastrointestinal nematode infection
