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作 者:Andrea K Erickson Michael Gale Jr
机构地区:[1]Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, 75235-9840, USA [2]Department of lmmunology, University of Washington School of Medicine, Seattle, WA, 98195-7650, USA
出 处:《Cell Research》2008年第4期433-435,共3页细胞研究(英文版)
摘 要:Innate intracellular immune programs mediate our first line of defense against virus infection and are dependent on type I interferon (IFNs) [1]. IFNs are cytokines that are produced and secreted from virus-infected cells. Autocrine and paracrine engagement by IFNs of the type I IFN receptor initiates tissue-wide and systemic signaling through the cellular Jak-STAT pathway to induce the transcription of hundreds of interferon-stimulated genes (ISGs) (Figure 1A). ISG products confer a variety of functions, including direct antiviral activity, immunomodulatory function, and metabolic control to limit virus infection and promote the adaptive immune resoonse.
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