IL17A and colorectal carcinoma: 37 in patients with CRC. They showed that breach of the gut epithelial barrier by tumor dysplasia induced an influx of commensal microbial products, resulting in the accumulation and activation of IL‐23‐producing inflammatory dendritic cells. This was sufficient to induce γδT17 polarisation of Vδ1+ intraepithelial lymphocytes, with γδ T cells identified as being the main cellular source of IL‐17 in human CRC.