Extended Data Fig. 8: IL-11 signalling in GBM-associated astrocytes.
From: Glioblastoma-instructed astrocytes suppress tumour-specific T cell immunity
(a,b) IL11 expression per cell type (a) and GBM subtype (b) in TCGA after cell-type deconvolution. (c) IL11 (left) and IL11RA expression by cell type in scRNA-seq22. (d) Spatially annotated bulk RNA-seq from Ivy Glioblastoma Atlas showing expression correlation of STAT3 signalling program (M5897) and TRAIL-driven apoptosis signalling (M23448) split by anatomical structure. (e) Spatial transcriptomics analysis of human GBM performed with SPATA286 showing spatially-weighted correlation of IL11 expression with GBM subtype metaprograms32. (f) IL11RA expression by time to recurrence in GBM-associated astrocytes analysed by scRNA-seq in Fig. 1b. (g) IL11RA expression in GBM-associated astrocytes determined by scRNA-seq. (h) Il11ra1 expression in GL261-associated astrocytes determined by scRNA-seq. (i-k) IL-11 quantified by ELISA in conditioned media from primary human GBM lines (i, n = 4 each), primary mouse astrocytes or GL261 cultures (j, n = 3 astrocytes, n = 6 GL261), or genetically-engineered glioma models (k, n = 4 each). (l) pSTAT3 (Y705) in primary murine astrocytes stimulated with rmIL-11 for 15 mins. (m) TNFSF10 promoter luciferase reporter activity in HepG2 cells treated with rhIL-11 for 24 or 48 h. (n) Tnfsf10 expression measured by qPCR in purified cultures of either microglia, oligodendrocytes, or neurons overnight with recombinant IL-11. (o) IL15 and TGFB1 expression in GBM cells analysed by scRNA-seq4. (p) Tnfsf10 expression measured by qPCR in primary mouse astrocyte cultures stimulated with the indicated cytokines. Data shown as mean ± SEM. Unpaired two-tailed t-test and two-way ANOVA used. n indicates biologically independent samples.
