Fig. 5: Increased cytotoxicity in CD16+ NK cells of PCV13 WRs.
a, Heat map of the differentially expressed genes in CD16+ NK cells of six PCV13 SRs and five WRs at baseline, as assessed using normalized expression values from the scRNA-seq pseudobulk analysis. b, Box plots comparing anti-CMV IgG titers between SRs and WRs for PCV13 (left) and PPSV23 (right). c, Correlation analysis of prevaccination CD16+ NK cell percentages estimated by scRNA-seq and CIBERSORTx (n = 11). d, Correlation analysis of CIBERSORTx-based estimates of CD16+ NK cells and PPSV23 rank (n = 16) at baseline. e, Correlation analysis of CD16+ NK cell percentages determined by scRNA-seq and TH1 and TH17 cell percentages determined using flow cytometry at baseline. f, Box plots of prevaccination CD16+ NK cell percentages in Fluad responders (R; n = 3) and non-responders (NR; n = 3) and Fluzone trivalent inactivated influenza vaccine responders (n = 5) and non-responders (n = 11). g, Summary schema showing the demographic, clinical, cellular and transcriptomic parameters associated with PCV13 and PPSV23 vaccine responsiveness at baseline and day 10. Box plots display the median and IQR (25–75%), with whiskers representing the upper and lower quartiles ±1.5× IQR. A Wilcoxon rank-sum test (two sided) was used to compare the mean anti-CMV IgG titers between SRs and WRs of PCV13 and PPSV13 donors (b) and prevaccination CD16+ NK cell percentages in Fluad responders and non-responders and Fluzone responders and non-responders (f). Correlation analyses were computed using the Pearson correlation metric (c, d and e), and P values were computed using two-sided t-tests; n represents the number of biological replicates.
