Many epithelial tumours respond poorly to immunotherapy, and the reasons for this are not well understood. Cancer-associated fibroblasts (CAFs) are the most frequent non-neoplastic cell type in most solid tumours, and are a major source of Transforming growth factor beta (TGFβ) which is central to immunotherapy resistance. Recent studies have demonstrated roles for stromal TGFβRII in immunosuppression in the tumour microenvironment and in immunotherapy-resistant cancer patients. We identified the TGFβ pathway as a significant mediator of CAF-driven T cell suppression, conserved across human colorectal, breast and pancreatic CAFs. Molecular inhibition of TGFβ signalling and deletion of CAF-TGFβRII each significantly reversed T cell suppression while ameliorating expected pathology-linked phenotypes including matrix remodelling. Using tumour organoids derived from colorectal carcinoma, we confirmed that suppression occurs in the presence of tumour organoids, and that T cell suppression is significantly lifted in the presence of TGFβRII knockout CAFs. RNA-seq and functional testing of human colorectal CAFs showed that TGFβ treatment promoted the development of a highly desmoplastic myofibroblastic CAF phenotype; while TGFβRII-/- CAFs displayed a cytokine-rich inflammatory CAF phenotype that was significantly less capable of inducing T cell suppression. These findings support a growing body of literature describing TGFβ and its receptor as a targetable T cell or stromal checkpoint that links CAF differentiation state to T cell suppression. This work illuminates new opportunities to overcome immunotherapy resistance through selective targeting of CAFs.