Progressive susceptibility to tumors and infectious diseases in the elderly are a serious threat to public health in aging societies. For this reason, there is growing interest in mechanisms and predictive biomarkers that accompany and potentially cause this process. In this issue of EMBO Reports, Chen et al [1] report the surprising finding that a specific subset of γδ T cells with very limited clonal diversity strongly expands in lymph nodes of aging mice. These T cells uniformly express a T-cell receptor (TCR) composed of a Vγ6 and a Vδ1 chain and show an effector T-cell phenotype characterized by the swift production of the pro-inflammatory cytokine interleukin-17 (IL-17) upon ex vivo stimulation (γδT17 cells). Since γδT17 cells are suspected to be pro-tumorigenic [2], the authors next compared how mice of different age coped with an experimental lung cancer challenge and found impaired anti-tumor responses in old mice. Based on these observations, they propose a link between changes of the composition of γδ T cells in the aging lymph nodes and increased risk of cancer development in aged mice.
