scholarly journals CD83 Expression Regulates Antibody Production in Response to Influenza A Virus Infection

2020 ◽  
Author(s):  
Madhav Akauliya ◽  
Avishekh Gautam ◽  
Sony Maharjan ◽  
Byoung Kwon Park ◽  
Jinsoo Kim ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Cell Population ◽  
Peritoneal Cavity ◽  
Antibody Production ◽  
Influenza A ◽  
Wild Type ◽  
Influenza A Virus Infection

Abstract Background: CD83 is known to regulate lymphocyte maturation, activation, homeostasis, and antibody response to immunization and infection. While CD83 has a major part in B cell function, its role in influenza A virus infection has not yet been investigated. Methods: We investigated the role of CD83 using C57BL/6J wild type mice and CD83 knockout (KO) mice after intraperitoneal administration of the influenza A/WSN/1933 virus. We analyzed cells of the peritoneal cavity, splenocytes, and cells of the bone marrow with FACS to investigate CD83 expression and cell population change in response to the virus infection. ELISA was performed with sera and peritoneal cavity fluids to detect A/WSN/1933 virus-specific IgG and the subclasses of IgG. Results: FACS analysis data showed a transient but distinct induction of CD83 expression in the peritoneal B cells of wild type mice. CD83 KO mice exhibited a delayed recovery of B cells in the bone marrow after influenza virus infection and overall, a smaller T cell population compared to wild type mice. The peritoneal cavity and serum of the wild type mice contained a high titer of IgG within 14 days after infection, whereas the CD83 KO mice had a very low titer of IgG. Conclusions: These results show the importance of CD83 in lymphocytes homeostasis and antibody production during influenza A virus infection.

scholarly journals CD83 expression regulates antibody production in response to influenza A virus infection

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Madhav Akauliya ◽  
Avishekh Gautam ◽  
Sony Maharjan ◽  
Byoung Kwon Park ◽  
Jinsoo Kim ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Cell Population ◽  
Peritoneal Cavity ◽  
Antibody Production ◽  
Influenza A ◽  
Wild Type ◽  
Influenza A Virus Infection

Abstract Background CD83 is known to regulate lymphocyte maturation, activation, homeostasis, and antibody response to immunization and infection. While CD83 has a major part in B cell function, its role in influenza A virus infection has not yet been investigated. Methods We investigated the role of CD83 using C57BL/6J wild type mice and CD83 knockout (KO) mice after intraperitoneal administration of the influenza A/WSN/1933 virus. We analyzed cells of the peritoneal cavity, splenocytes, and cells of the bone marrow with FACS to investigate CD83 expression and cell population change in response to the virus infection. ELISA was performed with sera and peritoneal cavity fluids to detect A/WSN/1933 virus-specific IgG and the subclasses of IgG. Results FACS analysis data showed a transient but distinct induction of CD83 expression in the peritoneal B cells of wild type mice. CD83 KO mice exhibited a delayed recovery of B cells in the bone marrow after influenza virus infection and overall, a smaller T cell population compared to wild type mice. The peritoneal cavity and serum of the wild type mice contained a high titer of IgG within 14 days after infection, whereas the CD83 KO mice had a very low titer of IgG. Conclusions These results show the importance of CD83 in lymphocytes homeostasis and antibody production during influenza A virus infection.

scholarly journals CD83 expression regulates antibody production in response to influenza A virus infection

2020 ◽  
Author(s):  
Madhav Akauliya ◽  
Avishekh Gautam ◽  
Sony Maharjan ◽  
Byoung Kwon Park ◽  
Jinsoo Kim ◽  
...  
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Cell Population ◽  
Peritoneal Cavity ◽  
Antibody Production ◽  
Influenza A ◽  
Wild Type ◽  
Influenza A Virus Infection

Abstract Background: CD83 is known to regulate lymphocyte maturation, activation, homeostasis, and antibody response to immunization and infection. While CD83 has a major part in B cell function, its role in influenza A virus infection has not yet been investigated. Methods: We investigated the role of CD83 using C57BL/6J wild type mice and CD83 knockout (KO) mice after intraperitoneal administration of the influenza A/WSN/1933 virus. We analyzed cells of the peritoneal cavity, splenocytes, and cells of the bone marrow with FACS to investigate CD83 expression and cell population change in response to the virus infection. ELISA was performed with sera and peritoneal cavity fluids to detect A/WSN/1933 virus-specific IgG and the subclasses of IgG. Results: FACS analysis data showed a transient but distinct induction of CD83 expression in the peritoneal B cells of wild type mice. CD83 KO mice exhibited a delayed recovery of B cells in the bone marrow after influenza virus infection and overall, a smaller T cell population compared to wild type mice. The peritoneal cavity and serum of the wild type mice contained a high titer of IgG within 14 days after infection, whereas the CD83 KO mice had a very low titer of IgG. Conclusions: These results show the importance of CD83 in lymphocytes homeostasis and antibody production during influenza A virus infection.

scholarly journals Role of Memory B Cells in Hemagglutinin-Specific Antibody Production Following Human Influenza A Virus Infection

Pathogens ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 167 ◽  
Author(s):  
Mark Y. Sangster ◽  
Phuong Q. T. Nguyen ◽  
David J. Topham
Keyword(s):  
B Cells ◽  
Virus Infection ◽  
Antibody Response ◽  
Influenza A Virus ◽  
Antibody Production ◽  
Specific Antibody ◽  
Germinal Center ◽  
Influenza A ◽  
Influenza Virus Infection

When influenza A virus infects an immune individual, preexisting memory B cell (MBC) activation and rapid anamnestic antibody production plays a key role in viral clearance. The most effective neutralizing antibodies target the antigenically variable head of the viral hemagglutinin (HA); antibodies against the conserved HA stalk provide broader but less potent protection. In this review, we provide a comprehensive picture of an adult’s HA-specific antibody response to influenza virus infection. The process is followed from preexisting HA-specific MBC activation and rapid production of anti-HA antibodies, through to germinal center seeding and adaptation of the response to novel features of the HA. A major focus of the review is the role of competition between preexisting MBCs in determining the character of the HA-reactive antibody response. HA novelty modifies this competition and can shift the response from the immunodominant head to the stalk. We suggest that antibodies resulting from preexisting MBC activation are important regulators of anti-HA antibody production and play a role in positive selection of germinal center B cells reactive to novel HA epitopes. Our review also considers the role of MBCs in the effects of early-life imprinting on HA head- and stalk-specific antibody responses to influenza infection. An understanding of the processes described in this review will guide development of vaccination strategies that provide broadly effective protection.

scholarly journals A Detrimental Effect of Interleukin-10 on Protective Pulmonary Humoral Immunity during Primary Influenza A Virus Infection

2010 ◽  
Vol 84 (10) ◽  
pp. 5007-5014 ◽  
Author(s):  
Keer Sun ◽  
Luisa Torres ◽  
Dennis W. Metzger
Keyword(s):  
T Cells ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Interleukin 10 ◽  
Viral Clearance ◽  
Wild Type ◽  
Passive Protection ◽  
Virus Specific Antibody ◽  
Influenza A Virus Infection

ABSTRACT Interleukin-10 (IL-10) is an important anti-inflammatory molecule that can cause immunosuppression and long-term pathogen persistence during chronic infection of mice with viruses such as lymphocytic choriomeningitis virus. However, its specific role in immunity to acute viral infections is not fully understood. We found that IL-10 plays a detrimental role in host responses to acute influenza A virus since IL-10−/− mice had improved viral clearance and survival after infection compared to wild-type mice. Enhanced viral clearance in IL-10−/− mice was not correlated with increased CD4+ or CD8+ T-cell recruitment into the lung but was correlated with increased pulmonary anti-influenza virus antibody titers, and this was dependent upon the presence of T cells, primarily CD4+ T cells. In addition, virus-specific antibody produced during the early stages of infection in the respiratory tract of IL-10−/− but not wild-type mice was sufficient to mediate passive protection against viral challenge of naïve mice. Complement was necessary for this antibody-mediated passive protection, but FcγR or neutrophil deficiency did not significantly influence viral clearance. Our results show that an absence of IL-10 at the time of primary infection leads to enhanced local virus-specific antibody production and, thus, increased protection against influenza A virus infection.

scholarly journals Heterosubtypic Immunity to Influenza A Virus Infection Requires B Cells but Not CD8+Cytotoxic T Lymphocytes

2001 ◽  
Vol 183 (3) ◽  
pp. 368-376 ◽  
Author(s):  
Huan H. Nguyen ◽  
Frederik W. van Ginkel ◽  
Huong L. Vu ◽  
Jerry R. McGhee ◽  
Jiri Mestecky
Keyword(s):  
B Cells ◽  
T Lymphocytes ◽  
Virus Infection ◽  
Influenza A Virus ◽  
Cytotoxic T Lymphocytes ◽  
Influenza A ◽  
Heterosubtypic Immunity ◽  
Influenza A Virus Infection

scholarly journals Induction of cyclophilin A by influenza A virus infection facilitates group A Streptococcus coinfection

Cell Reports ◽  
2021 ◽  
Vol 35 (7) ◽  
pp. 109159
Author(s):  
Xiaoyuan Bai ◽  
Wenxian Yang ◽  
Xiaohan Luan ◽  
Huizi Li ◽  
Heqiao Li ◽  
...  
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Influenza A ◽  
Group A Streptococcus ◽  
Cyclophilin A ◽  
Group A ◽  
Influenza A Virus Infection

scholarly journals Dicer is involved in protection against influenza A virus infection

2007 ◽  
Vol 88 (10) ◽  
pp. 2627-2635 ◽  
Author(s):  
Alexey A. Matskevich ◽  
Karin Moelling
Keyword(s):  
Virus Infection ◽  
Influenza A Virus ◽  
Mammalian Cells ◽  
Influenza A ◽  
Virus Production ◽  
Vero Cells ◽  
Antiviral Response ◽  
Protein Levels ◽  
Infected Cells ◽  
Influenza A Virus Infection

In mammals the interferon (IFN) system is a central innate antiviral defence mechanism, while the involvement of RNA interference (RNAi) in antiviral response against RNA viruses is uncertain. Here, we tested whether RNAi is involved in the antiviral response in mammalian cells. To investigate the role of RNAi in influenza A virus-infected cells in the absence of IFN, we used Vero cells that lack IFN-α and IFN-β genes. Our results demonstrate that knockdown of a key RNAi component, Dicer, led to a modest increase of virus production and accelerated apoptosis of influenza A virus-infected cells. These effects were much weaker in the presence of IFN. The results also show that in both Vero cells and the IFN-producing alveolar epithelial A549 cell line influenza A virus targets Dicer at mRNA and protein levels. Thus, RNAi is involved in antiviral response, and Dicer is important for protection against influenza A virus infection.

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