Supplementary Figures 1-23 from Immune Cell Abundance and T-cell Receptor Landscapes Suggest New Patient Stratification Strategies in Head and Neck Squamous Cell Carcinoma

Supplementary Figure 1 shows differences in immune cell infiltration/activity between the five immunity groups. Supplementary Figure 2 shows correlation in inferred cell abundance between distinct immune cell subpopulations in the TME of HNSCC tumours. Supplementary Figure 3 shows validation of immune phenotypes in n=520 HNSCC TCGA samples. Supplementary Figure 4 shows PD-L1 expression in TCGA immunity groups. Supplementary Figure 5 shows tumour microenvironment landscapes by HPV status. Supplementary Figure 6 shows differences in immune cell infiltration by HNSCC tumour sites of origin. Supplementary Figure 7 shows overall survival differences by immunity subgroup in the discovery cohort. Supplementary Figure 8 shows overall survival differences by immunity subgroup in the TCGA cohort (n=518). Supplementary Figure 9 shows differences in total mutational burden (log 10 scale) between the five immunity subgroups. Supplementary Figure 10 shows the tumour mutational burden is inversely correlated with the observed richness of the TCR repertoire. Supplementary Figure 11 shows exhaustion and TCR repertoire variation in relation to subclonality. Supplementary Figure 12 shows the top prevalent signatures in the cohort, as inferred by deconstructSigs. Supplementary Figure 13s shows somatic mutations across the Ras/MAPK and PI3K/AKT kinase signalling pathway components. Supplementary Figure 14 shows correlation between the expression of genes in the Ras/MAPK and PI3K/AKT pathway and TCR productive clonality. Supplementary Figure 15 shows correlation between the expression of genes in the Ras/MAPK and PI3K/AKT pathway and the observed richness of the TCR repertoire. Supplementary Figure 16 shows expression of 29 (out of 52) receptor tyrosine kinases and downstream genes in the MAPK/ERK and PI3K/AKT pathways was measurable using the Nanostring gene expression panel. Supplementary Figure 17 shows validation of EGFR expression trends by immunity group in TCGA. Supplementary Figure 18 shows modelling the two immunity classes (high/low) based on signalling of all measurable genes across tyrosine kinase pathways. Supplementary Figure 19 shows expression of markers associated with high cytotoxicity across the immunity groups. Supplementary Figure 20 shows expression of TLS-specific signature genes and chemokine signalling by HPV status. Supplementary Figure 21 shows IHC protein staining for CD8+/CD3+ T cells and Treg markers (FOXP3, GITR) by HPV status. Supplementary Figure 22 shows validation of TLS signature trends in TCGA. Supplementary Figure 23 shows the TLS signature score is weakly correlated with the productive clonality of the TCR repertoire.