Influenza virus infection expands the breadth of antibody responses through IL-4 signalling in B cells

Kosuke Miyauchi, Yu Adachi, Keisuke Tonouchi, Taiki Yajima, Yasuyo Harada, Hidehiro Fukuyama, Senka Deno, Yoichiro Iwakura, Akihiko Yoshimura, Hideki Hasegawa, Katsuyuki Yugi, Shin-ichiro Fujii, Osamu Ohara, Yoshimasa Takahashi and Masato Kubo ()
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Kosuke Miyauchi: Laboratory for Cytokine Regulation, Research Center for Integrative Medical Sciences (IMS), RIKEN Yokohama Institute
Yu Adachi: National Institute of Infectious Diseases
Keisuke Tonouchi: National Institute of Infectious Diseases
Taiki Yajima: Division of Molecular Pathology, Research Institute for Biomedical Science, Tokyo University of Science
Yasuyo Harada: Division of Molecular Pathology, Research Institute for Biomedical Science, Tokyo University of Science
Hidehiro Fukuyama: Laboratory for Lymphocyte Differentiation, Research Center for Integrative Medical Sciences (IMS), RIKEN Yokohama Institute
Senka Deno: Laboratory for Integrated Cellular Systems, Research Center for Integrative Medical Sciences (IMS), RIKEN Yokohama Institute
Yoichiro Iwakura: Center for Animal Disease Models, Research Institute for Biomedical Science, Tokyo University of Science
Akihiko Yoshimura: Keio University School of Medicine
Hideki Hasegawa: Influenza Virus Research Center, National Institute of Infectious Diseases
Katsuyuki Yugi: Laboratory for Integrated Cellular Systems, Research Center for Integrative Medical Sciences (IMS), RIKEN Yokohama Institute
Shin-ichiro Fujii: Laboratory for Immunotherapy, Research Center for Integrative Medical Sciences (IMS), RIKEN Yokohama Institute
Osamu Ohara: Laboratory for Integrative Genomics, Research Center for Integrative Medical Sciences (IMS), RIKEN Yokohama Institute
Yoshimasa Takahashi: National Institute of Infectious Diseases
Masato Kubo: Laboratory for Cytokine Regulation, Research Center for Integrative Medical Sciences (IMS), RIKEN Yokohama Institute

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract Influenza viruses are a major public health problem. Vaccines are the best available countermeasure to induce effective immunity against infection with seasonal influenza viruses; however, the breadth of antibody responses in infection versus vaccination is quite different. Here, we show that nasal infection controls two sequential processes to induce neutralizing IgG antibodies recognizing the hemagglutinin (HA) of heterotypic strains. The first is viral replication in the lung, which facilitates exposure of shared epitopes that are otherwise hidden from the immune system. The second process is the germinal center (GC) response, in particular, IL-4 derived from follicular helper T cells has an essential role in the expansion of rare GC-B cells recognizing the shared epitopes. Therefore, the combination of exposure of the shared epitopes and efficient proliferation of GC-B cells is critical for generating broadly-protective antibodies. These observations provide insight into mechanisms promoting broad protection from virus infection.

Date: 2021
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DOI: 10.1038/s41467-021-24090-z

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