Selected article for: "necrosis factor and tumor necrosis factor alpha TNFÎ"

Author: Rhein, Bethany A.; Powers, Linda S.; Rogers, Kai; Anantpadma, Manu; Singh, Brajesh K.; Sakurai, Yasuteru; Bair, Thomas; Miller-Hunt, Catherine; Sinn, Patrick; Davey, Robert A.; Monick, Martha M.; Maury, Wendy
Title: Interferon-? Inhibits Ebola Virus Infection
  • Document date: 2015_11_12
  • ID: 10bu7iwg_4
    Snippet: The ability of IFNs other than type I IFN to control EBOV infection has not been explored and several lines of reasoning suggest that type II IFN, interferon gamma (IFNγ), would inhibit EBOV infection of macrophages. Macrophages treated with IFNγ alone or in combination with tumor necrosis factor alpha (TNFα) are activated towards a M1 phenotype that is characteristically proinflammatory and antiviral, enhancing host defenses [14] [15] [16] . .....
    Document: The ability of IFNs other than type I IFN to control EBOV infection has not been explored and several lines of reasoning suggest that type II IFN, interferon gamma (IFNγ), would inhibit EBOV infection of macrophages. Macrophages treated with IFNγ alone or in combination with tumor necrosis factor alpha (TNFα) are activated towards a M1 phenotype that is characteristically proinflammatory and antiviral, enhancing host defenses [14] [15] [16] . As IFNγ directly stimulates the expression of a number of interferon-stimulated genes (ISGs) having antiviral activity [17, 18] , IFNγ treatment would be predicted to generate macrophages that are resistant to EBOV infection. Since it is thought that EBOV infection of macrophages is responsible for dysregulated cytokine production, reducing infection would likely reduce aberrant cytokine production concomitantly. Finally, as IFNγ potently activates T cell responses through enhancement of phagocytosis and antigen presentation [19] , such stimulation of antigen presentation would be predicted to enhance adaptive immune responses to in vivo infection.

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