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Only type-I interferon restricts viral replication of attenuated Measles virus (MV) Schwarz strain in mice, independently of the presence of hCD46 receptor.
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A key role of the IL7 and Interferon type I receptor axis in the regulation of intratumoral t-cell functions and in the development of primary breast tumor growth and metastasis.
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Data, including data from studies in knockout and double-knockout mice, suggest complex and sex-specific roles of Ifnar1 and Ifnar2 in type 1 diabetes (T1D); female NOD mice develop T1D in absence of both Ifnar1 and Ifnar2, whereas male mice do not.
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we uncovered that IFNAR1 expression in stromal benign cells functions to protect against progression of leukemia.
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Concurrent ablation of Ifnar1 led to a modest attenuation of the CK1alpha-null phenotype indicating that, although other CK1alpha targets are likely to be important, IFNAR1 downregulation can contribute to the maintenance of the HSCs function.
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Central nervous system signaling through IFNAR1 is a factor that is critical to neural injury after stroke.
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a deleterious role for the type-1 IFNs as key modulators of the early neuroinflammatory response and therefore the neuronal cell death in Parkinson's disease
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results clearly demonstrate that: (i) MHV-68, MHV-72 and MHV-4556 differentially interact with intracellular signaling and dysregulate IFN signal transduction; (ii) MHV-68, MHV-72 and MHV-4556 degrade type I IFN receptor in very early stages of infection (2-4hpi), but not type III IFN receptor
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Results show that removal of type-1 IFN signalling in the APPSWE/PS1DeltaE9 mouse model of AD confers a predominantly anti-inflammatory glial response and protects from cognitive decline. However this phenotype does not correlate with alterations in amyloid deposition and only a modest reduction in Abeta monomer levels.
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transfusion-induced differentiation of IFNAR1(-/-) B cells into germinal center B cells and plasma cells was significantly reduced, compared to WT B cells. This study demonstrates that B cells require signaling from IFN-alpha/beta to produce alloantibodies to the human KEL glycoprotein in mice.
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study provides evidence of STING activation in T cells, in which STING agonists not only provoke type I IFN production and IFN-stimulated gene expression, mirroring the response of innate cells, but are also capable of activating cell stress and death pathways.
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These data suggest that plasmacytoid dendritic cells producing IFN-alpha and IL-33 play a pivotal role in the chronic fibro-inflammatory responses underlying murine autoimmune pancreatitis and human IgG4-related autoimmune pancreatitis.
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type I interferons, besides their known antiviral properties, can initiate the recruitment and activation of leukocytes via induction of chemokine expression including CCL2.
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this study shows that the presence of IFN-alpha at antigen sensitization activates an IDO1/TGF-beta-dependent anti-inflammatory program that upon antigenic rechallenge prevents inflammation via plasmacytoid dendritic cells
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these studies demonstrate an important role for type I IFN in skin fibrosis, and they provide a rationale for IFNAR1 inhibition in scleroderma
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These results identify a key interface created by IFNAR1 residues Tyr(240) and Tyr(274) interacting with IFN-beta residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82) that underlie IFN-beta-IFNAR1-mediated signaling and biological processes.
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IFNAR1-deficiency accelerated humoral immune responses and parasite control by boosting ICOS-signalling in two non-lethal murine models of malaria
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reduced type I interferon production in obesity is caused by SOCS3 overexpression as well as tolerance induced by leptin
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These identify A129 mice as being highly susceptible to ZIKV and thus A129 mice represent a suitable, and urgently required, small animal model for the testing of vaccines and antivirals.
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Downregulation of IFNAR1 promotes melanoma development and progression. IFNAR1 mutation, which is partially resistant to downregulation, delays melanoma development.
