4.7 Article

Lung-Derived Exosomal miR-483-3p Regulates the Innate Immune Response to Influenza Virus Infection

期刊

JOURNAL OF INFECTIOUS DISEASES
卷 217, 期 9, 页码 1372-1382

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiy035

关键词

influenza virus; exosome; microRNA; innate immunity

资金

  1. Japan Science and Technology Agency
  2. Leading Advanced Projects for Medical Innovation from the Japan Agency for Medical Research and Development (AMED) [JP17am0001007]
  3. Japan Initiative for Global Research Network on Infectious Diseases from AMED
  4. Scientific Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science and Technology of Japan [16H06429, 16K21723, 16H06434]
  5. JSPS
  6. Joint Research Project of the Institute of Medical Science, University of Tokyo
  7. Grants-in-Aid for Scientific Research [16H06434, 16H06429] Funding Source: KAKEN

向作者/读者索取更多资源

Exosomes regulate cell-cell communication by transferring functional proteins and RNAs between cells. Here, to clarify the function of exosomes during influenza virus infection, we characterized lung-derived exosomal micro RNAs (miRNAs). Among the detected miRNAs, miR-483-3p was present at high levels in bronchoalveolar lavage fluid (BALF) exosomes during infection of mice with various strains of influenza virus, and miR-483-3p transfection potentiated gene expression of type I interferon and proinflammatory cytokine upon viral infection of MLE-12 cells. RNF5, a regulator of the RIG-I signaling pathway, was identified as a target gene of miR-483-3p. Moreover, we found that CD81, another miR-483-3p target, functions as a negative regulator of RIG-I signaling in MLE-12 cells. Taken together, this study indicates that BALF exosomal miRNAs may mediate the antiviral and inflammatory response to influenza virus infection.

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