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

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...

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Published inNature communications Vol. 12; no. 1; pp. 3789 - 15
Main Authors Miyauchi, Kosuke, Adachi, Yu, Tonouchi, Keisuke, Yajima, Taiki, Harada, Yasuyo, Fukuyama, Hidehiro, Deno, Senka, Iwakura, Yoichiro, Yoshimura, Akihiko, Hasegawa, Hideki, Yugi, Katsuyuki, Fujii, Shin-ichiro, Ohara, Osamu, Takahashi, Yoshimasa, Kubo, Masato
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 18.06.2021
Nature Publishing Group
Nature Portfolio
Subjects
13/1
13/31
38/23
631/250/127/1213
631/250/1619/40
631/250/2152/2153/1291
631/326/596/1578
Antibodies
Antibody response
Cell proliferation
Epitopes
Hemagglutinins
Humanities and Social Sciences
Immune system
Immunoglobulin G
Infections
Influenza
Interleukin 4
Lymphocytes
Lymphocytes B
Lymphocytes T
multidisciplinary
Public health
Science
Science (multidisciplinary)
Sinusitis
Vaccines
Viruses
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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. The reasons why influenza infection promotes a broader antibody response compared with vaccines are not fully understood. Here the authors show that unmasking of haemagglutinin epitopes and IL-4 signals in the germinal centre contribute to broader antibody responses after infection.
AbstractList 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.
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. The reasons why influenza infection promotes a broader antibody response compared with vaccines are not fully understood. Here the authors show that unmasking of haemagglutinin epitopes and IL-4 signals in the germinal centre contribute to broader antibody responses after infection.
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.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.
The reasons why influenza infection promotes a broader antibody response compared with vaccines are not fully understood. Here the authors show that unmasking of haemagglutinin epitopes and IL-4 signals in the germinal centre contribute to broader antibody responses after infection.
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.The reasons why influenza infection promotes a broader antibody response compared with vaccines are not fully understood. Here the authors show that unmasking of haemagglutinin epitopes and IL-4 signals in the germinal centre contribute to broader antibody responses after infection.
ArticleNumber 3789
Author Adachi, Yu
Yugi, Katsuyuki
Fujii, Shin-ichiro
Yoshimura, Akihiko
Ohara, Osamu
Miyauchi, Kosuke
Deno, Senka
Kubo, Masato
Tonouchi, Keisuke
Takahashi, Yoshimasa
Yajima, Taiki
Harada, Yasuyo
Fukuyama, Hidehiro
Iwakura, Yoichiro
Hasegawa, Hideki
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Snippet Influenza viruses are a major public health problem. Vaccines are the best available countermeasure to induce effective immunity against infection with...
The reasons why influenza infection promotes a broader antibody response compared with vaccines are not fully understood. Here the authors show that unmasking...
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Antibodies
Antibody response
Cell proliferation
Epitopes
Hemagglutinins
Humanities and Social Sciences
Immune system
Immunoglobulin G
Infections
Influenza
Interleukin 4
Lymphocytes
Lymphocytes B
Lymphocytes T
multidisciplinary
Public health
Science
Science (multidisciplinary)
Sinusitis
Vaccines
Viruses
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Title Influenza virus infection expands the breadth of antibody responses through IL-4 signalling in B cells
URI https://link.springer.com/article/10.1038/s41467-021-24090-z
https://www.proquest.com/docview/2542532420
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https://pubmed.ncbi.nlm.nih.gov/PMC8213721
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Volume 12
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