有哪些信誉好的足球投注网站host immune responses to a viral immune modulating protein immunogenicity of viral interleukin-10 in rhesus cytomegalovirus-infected rhesus macaques宿主免疫反应的病毒免疫调节蛋白的免疫原性,病毒在恒河cytomegalovirus-infected恒河猴白细胞介素- 10u201d.pdfVIP
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host immune responses to a viral immune modulating protein immunogenicity of viral interleukin-10 in rhesus cytomegalovirus-infected rhesus macaques宿主免疫反应的病毒免疫调节蛋白的免疫原性,病毒在恒河cytomegalovirus-infected恒河猴白细胞介素- 10u201d
Host Immune Responses to a Viral Immune Modulating Protein: Immunogenicity of Viral Interleukin-10 in Rhesus Cytomegalovirus-Infected Rhesus Macaques 1 1 2 1 2 Meghan K. Eberhardt , W. L. William Chang , Naomi J. Logsdon , Yujuan Yue , Mark R. Walter , Peter A. Barry1,3,4* 1 Center for Comparative Medicine, University of California Davis, Davis, California, United States of America, 2 Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, United States of America, 3 Department of Pathology and Laboratory Medicine, University of California Davis, Davis, California, United States of America, 4 California National Primate Research Center, University of California Davis, Davis, California, United States of America Abstract Background: Considerable evidence has accumulated that multiple viruses, bacteria, and protozoa manipulate interleukin- 10 (IL-10)-mediated signaling through the IL-10 receptor (IL-10R) in ways that could enable establishment of a persistent microbial infection. This suggests that inhibition of pathogen targeting of IL-10/IL-10R signaling could prevent microbial persistence. Human cytomegalovirus (HCMV) and rhesus cytomegalovirus (RhCMV) express a viral interleukin-10 (cmvIL-10 and rhcmvIL-10, respectively) with comparable immune modulating properties in vitro to that of their host’s cellular IL-10 (cIL-10). A prior study noted that rhcmvIL-10 alters innate and adaptive immunity to RhCMV in vivo, consistent with a central role for rhcmvIL-10 during acute virus-host interactions. Since cmvIL-10 and rhcmvIL-10 are extremely divergent from the cIL-10 of their respective hosts, vaccine-mediated neutralization of their function could inhibit establishment of viral persistence without inhibition of cIL
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