Fig. 2: AC484 increases mouse and human tumour cell sensitivity to IFNγ and enhances T cell activation and function in vitro.

a, Per cent growth inhibition of B16 tumour cells treated with AC484 with or without IFNγ (0.5 ng ml⁻¹) (n = 5). b, In vitro growth curve of control and Ptpn2/n1-null B16 cells with or without AC484 (1 µM) and with or without IFNγ (10 ng ml⁻¹) (n = 3). c, Heatmap showing transcriptional response to IFNγ (10 ng ml⁻¹) in control or Ptpn2/n1-null B16 cells with or without AC484 (10 μM) treatment. d,e, IFNγ-induced antigen presentation on B16-OVA cells left untreated (NTX) or treated with AC484 (0.1 µM). Representative histograms (d) and MFI ± s.e.m. of SIINFEKL–H2-K^b (e, n = 6). f, OT-I T cell-mediated B16-OVA tumour cell killing (n = 3). g, Activation (per cent of CD69-expressing CD8⁺ T cells, n = 6) and IFNγ production (n = 8) of anti-CD3/CD28-stimulated splenic pan T cells isolated from C57BL/6N mice. h, CD69 expression (MFI) of control, Ptpn2-null and Ptpn1-null mouse CD8⁺ T cells with or without anti-CD3/CD28 stimulation and with or without AC484. i–k, AC484 pathway engagement and immune activation in human whole blood. i, pSTAT5 in whole blood from healthy donors (n = 8) and from patients with cancer (n = 5 per indication) stimulated with IL-2. j, Normalized frequency of CD69-expressing T cells (n = 4) and IFNγ and TNF production (n = 5) in TCR-stimulated whole blood from healthy donors. k, Gene expression for top differentially expressed genes in PBMCs from TCR-stimulated healthy donor whole blood (n = 6). The relationship between dose and gene expression is significant (P < 0.05) for all genes. Error bars represent the mean ± s.e.m.

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