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IFN Receptor (ifn + receptor)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of IFN Receptor

  • i ifn receptor
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    Selected Abstracts

    Systemic increase in type,I interferon activity in Sjögren's syndrome: A putative role for plasmacytoid dendritic cells

    EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 7 2008
    Manon
    Abstract In the salivary glands of primary Sjögren's syndrome (pSjS) patients, type,I IFN activity is increased, but systemic levels of type,I IFN proteins are rarely detected. This study focused on the systemic activity of type,I IFN in pSjS, as well as the role of peripheral plasmacytoid dendritic cells (pDC). Monocytes obtained from pSjS patients showed an increased expression of 40,genes. Twenty-three of these genes (58%), including IFI27, IFITM1, IFIT3 and IFI44, were inducible by type,I IFN. pSjS serum had an enhanced capability of inducing IFI27, IFITM1, IFIT3 and IFI44 in the monocytic cell line THP-1, likely due to the action of IFN-,. This effect could be inhibited by blocking the type,I IFN receptor, supporting a high type,I IFN bioactivity in pSjS serum. In addition, circulatory pDC showed increased expression of CD40. This expression was correlated to the expression level of the type,I IFN-regulated genes IFI27 and IFITM1 in monocytes of the same individual. This study indicates that the increased type,I IFN activity observed in pSjS patients is not only a local but also a systemic phenomenon and points to pDC as a possible source of this activity. [source]

    Type,I interferon-dependent and -independent expression of tripartite motif proteins in immune cells

    EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 3 2008
    Ricardo Rajsbaum
    Abstract The tripartite motif (TRIM) proteins are important in a variety of cellular functions additional to anti-viral activity. We systematically analysed mRNA expression of representative TRIM molecules in mouse macrophages, myeloid and plasmacytoid dendritic cells, and a selection of CD4+ T cell subsets. We defined four clusters of TRIM genes based on their selective expression in these cells. The first group of TRIM genes was preferentially expressed in CD4+ T cells and contained the COS-FN3 motif previously shown to be involved in protein interactions. Additional TRIM genes were identified that showed up-regulation in macrophages and dendritic cells upon influenza virus infection in a type,I IFN-dependent manner, suggesting that they have anti-viral activity. In support of this notion, a subset of these TRIM molecules mapped to mouse chromosome,7, syntenic to human chromosome,11, where TRIM family members such as TRIM5, shown to have anti-viral activity, are localized. A distinct group of TRIM was constitutively expressed in plasmacytoid dendritic cells independently of viral infection or signalling through the type,I IFN receptor. Our findings on expression and regulation of TRIM genes in cells of the immune system that have different effector functions in innate and adaptive immune responses, may provide leads for determining functions of this diverse family of molecules. [source]

    Interferon-, mediates suppression of C-reactive protein: Explanation for muted C-reactive protein response in lupus flares?

    ARTHRITIS & RHEUMATISM, Issue 12 2009
    Helena Enocsson
    Objective C-reactive protein (CRP) is synthesized by hepatocytes in response to interleukin-6 (IL-6) during inflammation. Despite raised IL-6 levels and extensive systemic inflammation, serum CRP levels remain low during most viral infections and disease flares of systemic lupus erythematosus (SLE). Because both viral infections and SLE are characterized by high levels of interferon-, (IFN,), the aim of this study was to determine whether this cytokine can inhibit the induction of CRP. Methods The interference of all 12 IFN, subtypes with CRP promoter activity induced by IL-6 and IL-1, was studied in a CRP promoter, and luciferase reporter,transfected human hepatoma cell line, Hep-G2. CRP secretion by primary human hepatocytes was analyzed by enzyme-linked immunosorbent assay. Results CRP promoter activity was inhibited by all single IFN, subtypes, as well as by 2 different mixtures of biologically relevant IFN, subtypes. The most prominent effect was seen using a leukocyte-produced mixture of IFN, (56% inhibition at 1,000 IU/ml). The inhibitory effect of IFN, was confirmed in primary human hepatocytes. CRP promoter inhibition was dose dependent and mediated via the type I IFN receptor. Transferrin production and Hep-G2 proliferation/viability were not affected by IFN,. Conclusion The current study demonstrates that IFN, is an inhibitor of CRP promoter activity and CRP secretion. This finding concords with previous observations of up-regulated IFN, and a muted CRP response during SLE disease flares. Given the fundamental role of both IFN, and CRP in the immune response, our results are of importance for understanding the pathogenesis of SLE and may also contribute to understanding the differences in the CRP response between viral and bacterial infections. [source]

    Lupus-like disease and high interferon levels corresponding to trisomy of the type I interferon cluster on chromosome 9p

    ARTHRITIS & RHEUMATISM, Issue 5 2006
    Haoyang Zhuang
    Objective Systemic lupus erythematosus (SLE) is associated with type I interferons (IFNs) and can be induced by IFN, treatment. This study looked for evidence of autoimmunity in a pedigree consisting of 4 family members with a balanced translocation 9;21 and 2 members with an unbalanced translocation resulting in trisomy of the short (p) arm and part of the long (q) arm of chromosome 9. These latter 2 subjects had 3 copies of the IFN gene cluster. Methods Subjects were evaluated clinically and serologically for autoimmune disease. Expression levels of IFN,4, IFN,, the type I IFN,inducible gene Mx1, the type I IFN receptor, interleukin-6, and tumor necrosis factor , were determined by real-time polymerase chain reaction. Circulating plasmacytoid dendritic cells, the main IFN-producing cells, were quantified by flow cytometry. Results Both subjects with trisomy of chromosome 9p had a lupus-like syndrome with joint manifestations and antinuclear antibodies: one had anti-RNP and antiphospholipid autoantibodies, and the other had anti,Ro 60. The 3 family members with a balanced translocation 9;21 had no clinical or serologic evidence of autoimmunity, similar to that in relatives who were unaffected by the chromosomal translocation. In the 2 subjects with trisomy of 9p, high levels of IFN,/, (comparable with those found in patients with SLE), increased signaling through the IFN receptor (as indicated by high Mx1 expression), and low levels of circulating plasmacytoid dendritic cells (as observed in patients with SLE) were evident. These abnormalities were not seen in individuals with a balanced translocation. Conclusion Trisomy of the type I IFN cluster of chromosome 9p was associated with lupus-like autoimmunity and increased IFN,/, and IFN receptor signaling. The data support the idea that abnormal regulation of type I IFN production is involved in the pathogenesis of SLE. [source]