Structure and expression of a new murine interferon-alpha gene: MuIFN-αI9

Seif, Isabelle; Maeyer‐Guignard, Jaqueline De

doi:10.1016/0378-1119(86)90014-4

Cited by 25 publications

(5 citation statements)

References 37 publications

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“…There is a high degree of homology between the subtypes at the amino acid level with 80–95% homology between the IFN‐α subtypes and 50% homology with IFN‐β. Furthermore, the murine and human IFN gene families are highly analogous 7,8 with more than 70% homology in nucleotide sequence for the IFN‐α subtypes and 68% for the IFN‐β subtypes 9 . The IFN subtypes signal via a common receptor, composed of the IFNAR1 and IFNAR2 subunits leading to JAK‐STAT activation, the formation of ISGF3 and subsequent onset of gene expression 10 …”

Section: Introductionmentioning

confidence: 99%

Type I interferon gene therapy protects against cytomegalovirus‐induced myocarditis

2002

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SUMMARYType I interferons (IFNs) are produced early in response to viral infection and modulate adaptive immunity. Previously we demonstrated localized protection against murine cytomegalovirus (MCMV) infection in IFN DNA-inoculated mice. Here we examine the effect of seven IFN subtypes (IFNA1, A2, A4, A5, A6, A9 and B), administered by DNA inoculation, on systemic MCMV infection and myocarditis. IFN transgene expression altered the pathogenesis of MCMV infection with regard to virus titre and myocarditis. IFNA6 treatment reduced MCMV replication whilst IFNA5 and A2 enhanced virus replication. IFNA6, A9, and B treatment inhibited acute myocarditis. A T helper type 1-like, antibody and cytokine, response correlated with decreased virus titre and myocarditis. In addition, IFNA6 was able to reduce chronic cardiac inflammation. This research into the effectiveness of seven type I IFNs, using DNA gene therapy, highlights the need for correct subtype usage in the treatment of disease. We demonstrate effective subtypes for treatment in both the acute and chronic phases of MCMV infection and the resultant development of myocarditis.

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Section: Introductionmentioning

confidence: 99%

Type I interferon gene therapy protects against cytomegalovirus‐induced myocarditis

2002

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“…They are coded by an intronless multigene family clustered on murine chromosome 4 and in human chromosome 9. One IFN-␤ and multiple IFN-␣ genes were found in the mouse and human genomes (11,13,14,15,22,25,30,35,37,39,41,44,47,50). Other IFN-␣/␤ genes described include the murine limitin gene and the human IFN-gene, as well as the IFN-and IFN-ε/ genes that were found in both the human and murine genomes (Table 1) (2,9,24,32,46).…”

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confidence: 99%

Characterization of the Murine Alpha Interferon Gene Family

Pesch

Lanaya

Renauld

et al. 2004

J Virol

173

156

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Mouse and human genomes carry more than a dozen genes coding for closely related alpha interferon (IFN-␣) subtypes. IFN-␣, as well as IFN-␤, IFN-, IFN-, and limitin, are thought to bind the same receptor, raising the question of whether different IFN subtypes possess specific functions. As some confusion existed in the identity and characteristics of mouse IFN-␣ subtypes, the availability of data from the mouse genome sequence prompted us to characterize the murine IFN-␣ family. A total of 14 IFN-␣ genes were detected in the mouse genome, in addition to three IFN-␣ pseudogenes. Four IFN-␣ genes (IFN-␣1, IFN-␣7/10, IFN-␣8/6, and IFN-␣11) exhibited surprising allelic divergence between 129/Sv and C57BL/6 mice. All IFN-␣ subtypes were found to be stable at pH 2 and to exhibit antiviral activity. Interestingly, some IFN subtypes (IFN-␣4, IFN-␣11, IFN-␣12, IFN-␤, and limitin) showed higher biological activity levels than others, whereas IFN-␣7/10 exhibited lower activity. Most murine IFN-␣ turned out to be N-glycosylated. However, no correlation was found between N-glycosylation and activity. The various IFN-␣ subtypes displayed a good correlation between their antiviral and antiproliferative potencies, suggesting that IFN-␣ subtypes did not diverge primarily to acquire specific biological activities but probably evolved to acquire specific expression patterns. In L929 cells, IFN genes activated in response to poly(I•C) transfection or to viral infection were, however, similar.

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“…They are encoded by an intronless multigene family clustered on murine chromosome 4. To this date, 1 IFN-␤ and 13 IFN-␣ genes have been described in the mouse, including one pseudogene (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Classically, IFN-␣/␤ have been studied for their potent antiviral activity but they also exert various immunoregulatory functions such as regulation of major histocompatibility complex (MHC) class-I antigen expression, interleukin (IL)-12 and IL-15 production, and natural killer cell activation, which shape the adaptive immune response to an invading pathogen (12,13).…”

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confidence: 99%