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SARS-CoV-2-specicific humoral immunity in convalescent patients with mild COVID-19 is supported by CD4⁺ T-cell help and negatively correlated with Alphacoronavirus-specific antibody titer.

ABSTRACT: This study aimed at investigating the nature of SARS-CoV-2-specific immunity in patients with mild COVID-19 and sought to identify parameters most relevant for the generation of neutralizing antibody responses in convalescent COVID-19 patients. In the majority of the examined patients a cellular as well as humoral immune response directed to SARS-CoV-2 was detected. The finding of an anti-SARS-CoV-2-reactive cellular immune response in healthy individuals suggests a pre-existing immunity to various common cold HCoVs which share close homology with SARS-CoV-2. The humoral immunity to the S protein of SARS-CoV-2 detected in convalescent COVID-19 patients correlates with the presence of SARS-CoV-2-reactive CD4⁺ T cells expressing T_h1 cytokines. Remarkably, an inverse correlation of SARS-CoV-2 S protein-specific IgGs with HCoV-NL63 and HCoV-229E S1 protein-specific IgGs suggests that pre-existing immunity to Alphacoronaviruses might have had an inhibitory imprint on the immune response to SARS-CoV-2-infection in the examined patients with mild COVID-19.

SUBMITTER: Odendahl M

PROVIDER: S-EPMC9512529 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature

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SARS-CoV-2-specicific humoral immunity in convalescent patients with mild COVID-19 is supported by CD4<sup>+</sup> T-cell help and negatively correlated with Alphacoronavirus-specific antibody titer.

Odendahl Marcus M Endler Iris I Haubold Beate B Rodionov Roman N RN Bornstein Stefan R SR Tonn Torsten T

Immunology letters 20220927

This study aimed at investigating the nature of SARS-CoV-2-specific immunity in patients with mild COVID-19 and sought to identify parameters most relevant for the generation of neutralizing antibody responses in convalescent COVID-19 patients. In the majority of the examined patients a cellular as well as humoral immune response directed to SARS-CoV-2 was detected. The finding of an anti-SARS-CoV-2-reactive cellular immune response in healthy individuals suggests a pre-existing immunity to vari ...[more]

PMID: 36174771

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Project description:BackgroundMyasthenia gravis (MG) is an autoimmune disease characterized by pathogenic antibodies that target structures of the neuromuscular junction. The evidence suggests that the regulation of long noncoding RNAs (lncRNAs) that is mediated by transcription factors (TFs) plays a key role in the pathophysiology of MG. Nevertheless, the detailed molecular mechanisms of lncRNAs in MG remain largely undetermined.MethodsUsing microarray analysis, we analyzed the lncRNA levels in MG. By bioinformatics analysis, LINC01566 was found to potentially play an important role in MG. First, qRT‒PCR was performed to verify the LINC1566 expressions in MG patients. Then, fluorescence in situ hybridization was conducted to determine the localization of LINC01566 in CD4 + T cells. Finally, the impact of LINC01566 knockdown or overexpression on CD4 + T-cell function was also analyzed using flow cytometry and CCK-8 assay. A dual-luciferase reporter assay was used to validate the binding of the TF FOSL1 to the LINC01566 promoter.ResultsBased on the lncRNA microarray and differential expression analyses, we identified 563 differentially expressed (DE) lncRNAs, 450 DE mRNAs and 19 DE TFs in MG. We then constructed a lncRNA-TF-mRNA network. Through network analysis, we found that LINC01566 may play a crucial role in MG by regulating T-cell-related pathways. Further experiments indicated that LINC01566 is expressed at low levels in MG patients. Functionally, LINC01566 is primarily distributed in the nucleus and can facilitate CD4 + T-cell apoptosis and inhibit cell proliferation. Mechanistically, we hypothesized that LINC01566 may negatively regulate the expressions of DUSP3, CCR2, FADD, SIRPB1, LGALS3 and SIRPB1, which are involved in the T-cell activation pathway, to further influence the cellular proliferation and apoptosis in MG. Moreover, we found that the effect of LINC01566 on CD4 + T cells in MG was mediated by the TF FOSL1, and in vitro experiments indicated that FOSL1 can bind to the promoter region of LINC01566.ConclusionsIn summary, our research revealed the protective roles of LINC01566 in clinical samples and cellular experiments, illustrating the potential roles and mechanism by which FOSL1/LINC01566 negatively regulates CD4 + T-cell activation in MG.

Dataset Information

SARS-CoV-2-specicific humoral immunity in convalescent patients with mild COVID-19 is supported by CD4⁺ T-cell help and negatively correlated with Alphacoronavirus-specific antibody titer.

Publications

SARS-CoV-2-specicific humoral immunity in convalescent patients with mild COVID-19 is supported by CD4<sup>+</sup> T-cell help and negatively correlated with Alphacoronavirus-specific antibody titer.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

SARS-CoV-2-specicific humoral immunity in convalescent patients with mild COVID-19 is supported by CD4+ T-cell help and negatively correlated with Alphacoronavirus-specific antibody titer.

Publications

SARS-CoV-2-specicific humoral immunity in convalescent patients with mild COVID-19 is supported by CD4<sup>+</sup> T-cell help and negatively correlated with Alphacoronavirus-specific antibody titer.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

SARS-CoV-2-specicific humoral immunity in convalescent patients with mild COVID-19 is supported by CD4⁺ T-cell help and negatively correlated with Alphacoronavirus-specific antibody titer.