Figure 1.

Immune signature of TME impacts survival of patients with OPSCC. (A) Kaplan-Meier survival curves of prospectively followed up cohort of HPV⁻ and HPV16⁺ patients with OPSCC, the latter of whom are also subdivided into those with a tumor-specific T-cell response (HPV16⁺IR⁺) and those lacking this immune response (HPV16⁺IR⁻). (B) Volcano plots of upregulated DEGs identified by NanoString Pancancer IO360 between HPV16⁺IR⁺ (right) and HPV16⁺IR⁻ (left). The dotted lines indicate the Benjamini-Hochberg adjusted p<0.05 and p<0.1 thresholds. (C) ClueGo of DEGs (p<0.1) between HPV16⁺IR⁺ and HPV16⁺IR⁻ patients, visualizing the pathways in which these genes are involved. (D) Deconvoluted cells by expression of genes predefined for different immune cell types depicted as counts in HPV⁻, HPV16⁺IR⁻ and HPV16⁺IR⁺ OPSCC. (E) Differential expression of predefined pathway genes in HPV⁻, HPV16⁺IR⁻ and HPV16⁺IR⁺ OPSCC. (F) Kaplan-Meier survival curves based on high/low LTB expression (classification based on median LTB expression), in all patients with OPSCC analyzed by NanoString Pancancer IO360 (n=21), in the HPV16⁺ patients within this cohort (n=13) and in a large independent TCGA cohort of HPV16⁺ OPSCC (n=69). (G) Linear regression analyses of top upregulated DEG LTB in HPV16⁺IR⁺ compared with HPV16⁺IR⁻ OPSCC versus cell-type profiles of CD8 (CD8A), CD4, Tbet⁺ T cells (TBX21) and DC (ITGAX, CD11c) both for this cohort (n=21, upper panel) and the TCGA cohort of HPV16⁺ OPSCC (n=69, lower panel). HPV⁻ (red), HPV16⁺IR⁻ (blue) and HPV16⁺IR⁺ (green). DC, dendritic cell; DEG, differentially expressed gene; HPV, human papillomavirus; IR⁺, immune responsiveness; IR⁻, lack of immune responsiveness; OPSCC, oropharyngeal squamous cell carcinoma; TCGA, The Cancer Genome Atlas; TME, tumor microenvironment.