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Capture of influenza by medullary dendritic cells via SIGN-R1 is essential for humoral immunity in draining lymph nodes

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  • Santiago F. Gonzalez, Immune Disease Institute, Harvard Medical School
  • ,
  • Veronika Lukacs-Kornek, Dana-Farber Cancer Institute
  • ,
  • Michael P. Kuligowski, Immune Disease Institute, Harvard Medical School
  • ,
  • Lisa A. Pitcher, Immune Disease Institute, Harvard Medical School
  • ,
  • Søren Egedal Degn
  • Young-A Kim, Immune Disease Institute, Harvard Medical School
  • ,
  • Mary J. Cloninger, Department of Chemistry and Biochemistry, Montana State University
  • ,
  • Luisa Martinez-Pomares, School of Molecular Medical Sciences, University of Nottingham
  • ,
  • Siamon Gordon, Sir William Dunn School of Pathology, University of Oxford
  • ,
  • Shannon J. Turley, Dana-Farber Cancer Institute
  • ,
  • Michael C. Carroll, Immune Disease Institute, Harvard Medical School
  • Department of Medical Microbiology and Immunology
A major pathway for B cell acquisition of lymph-borne particulate antigens relies on antigen capture by subcapsular sinus macrophages of the lymph node. Here we tested whether this mechanism is also important for humoral immunity to inactivated influenza virus. By multiple approaches, including multiphoton intravital imaging, we found that antigen capture by sinus-lining macrophages was important for limiting the systemic spread of virus but not for the generation of influenza-specific humoral immunity. Instead, we found that dendritic cells residing in the lymph node medulla use the lectin receptor SIGN-R1 to capture lymph-borne influenza virus and promote humoral immunity. Thus, our results have important implications for the generation of durable humoral immunity to viral pathogens through vaccination.
Original languageEnglish
JournalNature Immunology
Volume11
Issue5
Pages (from-to)427-435
Number of pages9
ISSN1529-2908
Publication statusPublished - May 2010

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