Figure 3 Natural and imatinib-induced immunosurveillance in gastrointestinal tumours (GISTs) Figure 3 | Natural and imatinib-induced immunosurveillance.

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Figure 3 Natural and imatinib-induced immunosurveillance in gastrointestinal tumours (GISTs) Figure 3 | Natural and imatinib-induced immunosurveillance in gastrointestinal tumours (GISTs). a | Natural immunosurveillance in GIST. GIST contain regulatory T (TREG) cells, as well as CD4+ type 1 helper T cells (TH1), CD8+ type 1 cytotoxic T cells (TC1 cells) located in the tumour nests surrounded by CD56bright CD16dim/− natural killer (NK) cells. b | Effects of imatinib on the tumour microenvironment. Imatinib promotes a loss of MHC class I molecules, which might reflect the T-cell-mediated elimination of MHC-I-positive tumour cells and hence an example of 'immunoediting'. Imatinib can reduce intratumoural TREG-cell numbers and cause a relocation of NK cells from the stroma to tumour foci, leading to a marked increase of the NK:TREG cell ratio in situ. The imatinib-induced increase of the NK:TREG-cell ratio is more pronounced in the subset of GIST harbouring an exon 11 KIT mutation83. Kroemer, G. et al. (2016) Immunological off-target effects of imatinib Nat. Rev. Clin. Oncol. doi:10.1038/nrclinonc.2016.41