Human Vγ9Vδ2 T cells are potent anti‐tumor lymphocytes that specifically respond to pyrophosphate (phospho‐) antigens, which constitute the basis of current γδ T‐cell‐based immunotherapy strategies. Despite a clear involvement of the TCR, the costimulation requirements of Vγ9Vδ2 T cells remain ill‐defined. Here, we show that the expression of the CD27 receptor by the vast majority of Vγ9Vδ2 peripheral blood lymphocytes endows them with enhanced proliferative capacity upon ligation by its unique ligand CD70, a tumor necrosis factor superfamily member expressed on lymphoma B‐cells but also on TCR‐activated γδ T cells. Moreover, Vγ9Vδ2 T‐cell treatment with soluble recombinant CD70 induced calcium signals and increased transcription of anti‐apoptotic Bcl2a1 and cell‐cycle‐promoting Cyclin D2 genes. We further demonstrate that the manipulation of CD70–CD27 interactions significantly impacted on Vγ9Vδ2 T‐cell survival, proliferation and cytokine secretion, in both loss‐of‐function and gain‐of‐function experiments. Thus, CD27 coreceptor signals strongly promoted the expansion of Th1‐biased, CD27⁺ Vγ9Vδ2 peripheral blood lymphocytes in the context of TCR‐mediated stimulation with phosphoantigens. These data collectively establish a novel role for the CD70–CD27 axis in human γδ T‐cell activation and hence open new perspectives for its modulation in clinical settings.