Requirement for memory B-cell activation in protection from heterologous influenza virus reinfection
Memory B cells protect against heterologous influenza infection Abstract While two memory compartments, memory B cells and long-lived plasma cells, are thought to contribute to the successful establishment of memory recall responses, the unique roles of each cellular compartment are still unclear. H...
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Published in | International immunology Vol. 31; no. 12; pp. 771 - 779 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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UK
Oxford University Press
08.11.2019
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Abstract | Memory B cells protect against heterologous influenza infection
Abstract
While two memory compartments, memory B cells and long-lived plasma cells, are thought to contribute to the successful establishment of memory recall responses, the unique roles of each cellular compartment are still unclear. Herein, by tracing influenza anti-hemagglutinin (HA)-specific antibodies in mice, we demonstrate that pre-existing antibodies secreted by long-lived plasma cells are essential for protection from reinfection with the same influenza virus, whereas protection from secondary infection with an antigenically distinct influenza virus requires memory B-cell activation. These activated memory B cells were largely specific for the conserved HA stem region, and generated sufficient levels of antibodies for protection from heterologous reinfection. Given that the anti-stem plasmablasts derived from the memory B cells were higher affinity than those from naive B cells, our results suggest that maturation of anti-stem memory B cells during primary influenza infection and their subsequent activation are required for protection from reinfection by mutant viruses. |
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AbstractList | Memory B cells protect against heterologous influenza infection
Abstract
While two memory compartments, memory B cells and long-lived plasma cells, are thought to contribute to the successful establishment of memory recall responses, the unique roles of each cellular compartment are still unclear. Herein, by tracing influenza anti-hemagglutinin (HA)-specific antibodies in mice, we demonstrate that pre-existing antibodies secreted by long-lived plasma cells are essential for protection from reinfection with the same influenza virus, whereas protection from secondary infection with an antigenically distinct influenza virus requires memory B-cell activation. These activated memory B cells were largely specific for the conserved HA stem region, and generated sufficient levels of antibodies for protection from heterologous reinfection. Given that the anti-stem plasmablasts derived from the memory B cells were higher affinity than those from naive B cells, our results suggest that maturation of anti-stem memory B cells during primary influenza infection and their subsequent activation are required for protection from reinfection by mutant viruses. While two memory compartments, memory B cells and long-lived plasma cells, are thought to contribute to the successful establishment of memory recall responses, the unique roles of each cellular compartment are still unclear. Herein, by tracing influenza anti-hemagglutinin (HA)-specific antibodies in mice, we demonstrate that pre-existing antibodies secreted by long-lived plasma cells are essential for protection from reinfection with the same influenza virus, whereas protection from secondary infection with an antigenically distinct influenza virus requires memory B-cell activation. These activated memory B cells were largely specific for the conserved HA stem region, and generated sufficient levels of antibodies for protection from heterologous reinfection. Given that the anti-stem plasmablasts derived from the memory B cells were higher affinity than those from naive B cells, our results suggest that maturation of anti-stem memory B cells during primary influenza infection and their subsequent activation are required for protection from reinfection by mutant viruses. While two memory compartments, memory B cells and long-lived plasma cells, are thought to contribute to the successful establishment of memory recall responses, the unique roles of each cellular compartment are still unclear. Herein, by tracing influenza anti-hemagglutinin (HA)-specific antibodies in mice, we demonstrate that pre-existing antibodies secreted by long-lived plasma cells are essential for protection from reinfection with the same influenza virus, whereas protection from secondary infection with an antigenically distinct influenza virus requires memory B-cell activation. These activated memory B cells were largely specific for the conserved HA stem region, and generated sufficient levels of antibodies for protection from heterologous reinfection. Given that the anti-stem plasmablasts derived from the memory B cells were higher affinity than those from naive B cells, our results suggest that maturation of anti-stem memory B cells during primary influenza infection and their subsequent activation are required for protection from reinfection by mutant viruses.While two memory compartments, memory B cells and long-lived plasma cells, are thought to contribute to the successful establishment of memory recall responses, the unique roles of each cellular compartment are still unclear. Herein, by tracing influenza anti-hemagglutinin (HA)-specific antibodies in mice, we demonstrate that pre-existing antibodies secreted by long-lived plasma cells are essential for protection from reinfection with the same influenza virus, whereas protection from secondary infection with an antigenically distinct influenza virus requires memory B-cell activation. These activated memory B cells were largely specific for the conserved HA stem region, and generated sufficient levels of antibodies for protection from heterologous reinfection. Given that the anti-stem plasmablasts derived from the memory B cells were higher affinity than those from naive B cells, our results suggest that maturation of anti-stem memory B cells during primary influenza infection and their subsequent activation are required for protection from reinfection by mutant viruses. |
Author | Leach, Sarah Takahashi, Yoshimasa Yamamoto, Takuya Adachi, Yu Fukuyama, Hidehiro Momota, Masatoshi Makino-Okamura, Chieko Ishii, Ken J Shinnakasu, Ryo Kurosaki, Tomohiro |
Author_xml | – sequence: 1 givenname: Sarah surname: Leach fullname: Leach, Sarah organization: Graduate School of Frontier Biosciences, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan – sequence: 2 givenname: Ryo orcidid: 0000-0002-5369-3424 surname: Shinnakasu fullname: Shinnakasu, Ryo email: ryoshin@ifrec.osaka-u.ac.jp organization: Laboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan – sequence: 3 givenname: Yu surname: Adachi fullname: Adachi, Yu organization: Department of Immunology, National Institute of Infectious Diseases, Tokyo, Japan – sequence: 4 givenname: Masatoshi surname: Momota fullname: Momota, Masatoshi organization: Laboratory of Adjuvant Innovation, National Institute of Biomedical Innovation, Osaka, Japan – sequence: 5 givenname: Chieko surname: Makino-Okamura fullname: Makino-Okamura, Chieko organization: Laboratory of Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa, Japan – sequence: 6 givenname: Takuya surname: Yamamoto fullname: Yamamoto, Takuya organization: Laboratory of Immunosenescence, National Institute of Biomedical Innovation, Osaka, Japan – sequence: 7 givenname: Ken J orcidid: 0000-0002-6728-3872 surname: Ishii fullname: Ishii, Ken J organization: Laboratory of Adjuvant Innovation, National Institute of Biomedical Innovation, Osaka, Japan – sequence: 8 givenname: Hidehiro surname: Fukuyama fullname: Fukuyama, Hidehiro organization: Laboratory of Lymphocyte Differentiation, RIKEN Center for Integrative Medical Sciences (IMS), Yokohama, Kanagawa, Japan – sequence: 9 givenname: Yoshimasa surname: Takahashi fullname: Takahashi, Yoshimasa organization: Department of Immunology, National Institute of Infectious Diseases, Tokyo, Japan – sequence: 10 givenname: Tomohiro surname: Kurosaki fullname: Kurosaki, Tomohiro organization: Graduate School of Frontier Biosciences, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan |
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Snippet | Memory B cells protect against heterologous influenza infection
Abstract
While two memory compartments, memory B cells and long-lived plasma cells, are thought... While two memory compartments, memory B cells and long-lived plasma cells, are thought to contribute to the successful establishment of memory recall... |
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SubjectTerms | Animals B-Lymphocytes - immunology B-Lymphocytes - metabolism Immunologic Memory - immunology Lymphocyte Activation - immunology Macrophages - immunology Macrophages - metabolism Mice Mice, Inbred BALB C Mice, Inbred C57BL Orthomyxoviridae - immunology Orthomyxoviridae - physiology |
Title | Requirement for memory B-cell activation in protection from heterologous influenza virus reinfection |
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