Immune characteristics analysis reveals two key inflammatory factors correlated to the expressions of SARS-CoV-2 S1-specific antibodies.

Abstract

The pandemic of COVID-19 caused by SARS-CoV-2 has made serious threats to the public health. Antibodies have been considered as promising therapeutics for the prevention and treatment of pathogens. So far, effectors that can influence the sustainability of SARS-CoV-2 specific antibodies in COVID-19 patients are still unclear. In this paper, we attempted to find potential key factors correlated with SARS-CoV-2 specific antibodies. Transcriptional analysis with the peripheral blood mononuclear cells (PBMCs) revealed proportional changes of immune cell subsets in COVID-19 convalescent patients, including a substantial decrease of monocytes and evident increase of dendritic cells (DCs). Moreover, we found that the gene expressions of chemokines associated with monocyte/macrophage were significantly up-regulated during the COVID-19 recovery phase. Most importantly, we found a set of 27 immune genes corresponding to a comparatively lower amount of SARS-CoV-2 specific antibodies, and identified two hub genes, IL1β and IL6, the protein expressions of which exhibited negative correlation with the immunoglobulin G (IgG) levels in COVID-19 convalescent sera. In addition, we found that high expressions of these 2 hub genes during the convalescent stage were negatively associated with the plasma cell marker CD138. Our study presented two key inflammatory factors correlated to the low level of SARS-CoV-2 specific antibodies, which indicated the potential regulatory process of plasmatic antibodies levels in some COVID-19 convalescent patients.

• Authors: Shenglong Li, Wang Wang, Tingting Li, Xiaojian Han, Chao Hu, Yingming Wang, Meiying Shen, Li Du, Yaru Nai, Jianwei Wang, Aishun Jin
• Journal: Genes & diseases (Genes Dis) Vol. 9 Issue 2 Pg. 522-530 (Mar 2022) ISSN: 2352-3042 [Electronic] Netherlands
• PMID: 33521209 (Publication Type: Journal Article)
• Copyright: © 2020 Chongqing Medical University. Production and hosting by Elsevier B.V.