CD83 expression regulates antibody production in response to influenza A virus infection
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RESEARCH
CD83 expression regulates antibody production in response to influenza A virus infection Madhav Akauliya1†, Avishekh Gautam1†, Sony Maharjan2, Byoung Kwon Park2, Jinsoo Kim1 and Hyung‑Joo Kwon1,2*
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, spleno‑ cytes, 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 infec‑ tion 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. Keywords: Antibody production, B cells, CD83, Influenza A virus, Peritoneal cavity Background CD83, an evolutionary conserved member of immunoglobulin, is a highly glycosylated type 1 transmembrane glycoprotein composed of 175 amino acids in mice [1] and 186 amino acids in humans [2]. CD83 consists of a variable extracellular Ig-like domain, transmembrane
*Correspondence: [email protected] † Madhav Akauliya and Avishekh Gautam have contributed equally to this work. 1 Department of Microbiology, College of Medicine, Hallym University, Chuncheon 24252, Republic of Korea Full list of author information is available at the end of the article
(TM) domain, and intracellular C-terminal cytoplasmic domain sharing 63% homology of amino acids between mice and humans [3]. CD83 is expressed in mature dendritic cells (DCs) and is an activation marker for DCs [3]. However, CD83 is also expressed in natural killer cells [4], activated macrophages [5, 6], neutrophils [7, 8], and activated T cells and B cells [2, 9–11]. CD83 is also expressed on thymic epithelial cells, where it contributes to the selective development and maturation of CD4+ T cells [12]. The TM domain of CD83 promotes and stabilizes the cell surface expression of major histocompatibility complex II (MHC II) and CD86 on DCs by inhibiting their
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