γδT cells are emerging as a potent antitumor innate immune population for cell-based immunotherapy. Although they recognise and kill cancerous cells, γδ T cells also express inhibitory receptors. Unravelling the complement of inhibitory receptors on γδT cell subsets may highlight therapeutic targets complementing their potential for cell-based immunotherapy. We characterised inhibitory receptor expression on human Vδ1, Vδ2 and Vδ3 γδ T cells in cord blood (CB), adult blood (AB) and endometrial tumours by flow cytometry. CB Vδ1 cells constitutively express PD1, whereas, TIGIT expression was low in CB versus AB (n=9, p<0.0003) and high at end-stage differentiation in AB. The majority of TIGIT+Vδ1 cells in endometrial tumours are TEM, whereas, in blood are TEMRA. We hypothesised TIGIT engagement may prevent progression to end-stage differentiation. To test this, we engaged TIGIT with an agonist which significantly (n=6, p<0.0001) decreased the proliferative capacity of TEM TIGIT+ Vδ1 cells from blood. We used the Cancer Genome Atlas RNA-Seq data of 373 endometrial cancer patients to reveal significantly (p=0.001) better overall survival of patients with high tumour gene expression for TRDV1 (Vδ1) and TIGIT. Comparing high and low TRDV1 and TIGIT expression, patient cohorts with high expression had significantly enriched immune KEGG pathways (p<0.05); such as NK cell mediated cytotoxicity and antigen processing and presentation. Flow cytometry revealed endometrial tumour TIGIT+Vδ1 cells maintain granzyme B levels versus blood. These results indicate TIGIT+Vδ1+ tumours could be ‘hot’, have a cytotoxic signature and good prognosis, suggesting potential benefits of combined checkpoint blockade and Vδ1 cell-based immunotherapy.