Phenotypes and Functions of Dendritic Cells in SARS-CoV-2 Vaccine-derived Humoral Immunity
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Le résumé fourni par la source
Abstract DCs regulate humoral immunity against SARS-CoV-2 by regulating CD4 + T cell activation, but the relations between DC phenotypes and functions and anti-RBD antibodies are unclear. We conducted this observational study in Huashan Hospital using a third 6.5U BBIBP-CorV or 25 µg ZF2001 administered at an interval of 4 to 8 months following the previous two doses in healthy adults. anti-RBD response and neutralizing titers against SARS-CoV-2 and VOCs were examined. DC maturation markers and pattern recognition receptors and cytokines produced by DC were measured, and DC function was tested in mixed lymphocyte reaction(MLR). Mean anti-RBD Ab and IgG rose from 22.08 and 9.17 on D0 to 4704.18 and 798.11 on D14(BAU/ml). Meanwhile, the surrogate virus neutralization test(sVNT) elevated from 17.15 on D0 to 2538.83 on D14. The expression of DC maturation markers on D3 and MLR were negatively correlated to sVNT, anti-RBD antibody, and IgG titers on D14(Spearman r=-0.558~-0.326) and D28(Spearman r=-0.615~-0.397), but positively correlated to IgG/Ab ratio(Spearman r = 0.249 ~ 0.509). DC function in activating T cells was also negatively related to anti-RBD antibody titer on D28(r=-0.532~-0.453, p = 0.015 ~ 0.035), and positively correlated with the proportion of anti-RBD IgG in Ab(r = 0.490 ~ 0.561, p = 0.010 ~ 0.032). DC-SIGN level showed a relation to antibody titer and IgG proportion opposite to DC maturation and function and was negatively related to the level of IL-10 produced by DCs. Our research suggested that DCs controlled CD4 + T cells in differentiating into regular T cells, and DC-SIGN might restrain T regular cells by suppressing IL-10 production of DC in anti-SARS-CoV-2 vaccination.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Phenotypes and Functions of Dendritic Cells in SARS-CoV-2 Vaccine-derived Humoral Immunity
- Date Crossref
- 04/08/2022
- Éditeur
- Research Square Platform LLC
- Type
- posted-content
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