RESUMO
Using single-cell proteomics by mass cytometry, we investigate changes to a broad selection of over 10,000,000 immune cells in a cohort of moderate, severe, and critical Japanese COVID-19 patients and healthy controls with a particular focus on regulatory T-cells (Tregs). We find significant disruption within all compartments of the immune system and the emergence of atypical CTLA-4high CD4 T-cells and proliferating HLA-DRlowCD38high Tregs associated with critical patients. We also observed disrupted regulation of humoral immunity in COVID-19, with a loss of circulating T follicular regulatory T cells (Tfr) and altered T follicular helper (Tfh)/Tfr and plasma cell/Tfr ratios, all of which are significantly lower in male patients. Shifting ratios of CXCR4 and CXCR5 expression in B-cells provides further evidence of an autoimmune phenotype and dysregulated humoral immunity. These results suggest that Tregs are central to the changing cellular networks of a wide range of cells in COVID-19 and that sex specific differences to the balance of Tfr, Tfh and plasma cells may have important implications for the specificity of the humoral immune response to SARS-CoV-2.
RESUMO
The humoral immune response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) plays a pivotal role in controlling coronavirus disease 2019 (COVID-19) infections. However, little is known about the persistence of the antibody response. We evaluated that the kinetics of anti-nucleocapsid protein antibody of SARS-CoV2 infected healthcare workers in COVID-19 cluster occurred hospital. The long-term kinetics of anti-N antibody was classified high and keep pattern, high and decay pattern, and low and keep pattern. COVID-19 contact and symptomaticity was not related to kinetic patterns. The reason of kinetic difference was still unclear. However natural anti-SARS-CoV-2 antibody persistence was not uniform, suggesting inter-individual difference of SARS-CoV2 vaccine efficacy.
