Extended Data Fig. 2: Enhanced effector function response in LTBI.

a, Cell subsets, shown as red nodes in a Citrus-derived circular dendrogram and designated as 1–5, were identified as significantly different in abundance (SAM analysis at FDR < 1%) based on CyTOF analysis of effector and cell-surface molecule expression on PBMCs (antibody panel 1, Supplementary Table 2) from uninfected controls and individuals with LTBI (n = 14 per group) after 4-h PMA and ionomycin stimulation. Mapping of individual cell clusters to established, gross-cell types are identified by annotated shaded background groupings. b, Expression intensity of selected effector molecules is indicated by the coloured gradient for which the range corresponds to the arcsinh-transformed expression of the median marker expression measured across all Citrus clusters. c, Effector molecule expression and the composition of cells in each of the stratifying cell clusters (1–5), identified by Citrus analysis. d, viSNE analysis of GZMB expression level in immune-cell subsets, representative of 14 uninfected and 14 individuals with LTBI (the colour gradient corresponds to the arcsinh-transformed expression level). e, Quantification of intracellular GZMB expression level in NK cells, CD8⁺ αβ T cells and γδ T cells in uninfected controls and individuals with LTBI (n = 14 per group). P values were derived using a Mann–Whitney U-test. Mean and error bars representing the 95% confidence intervals are shown for each comparison. f, Dot plots from CyTOF analysis of CD16⁺GZMB^high cells within each lymphocyte subset, representative of 14 uninfected controls and 14 individuals with LTBI. g, Gating strategy for ADCC. ADCC was measured using NK-resistant P815 cells, which were either coated with antibody (2.4G2) or left uncoated (control), and labelled with the intracellular dye CFSE, followed by the DNA dye 7AAD. CFSE⁺7AAD⁺ cells were defined as dead target cells.