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Are human Vδ2pos T cells really resistant to aging and Human Cytomegalovirus infection?


In their recent paper, Weili Xu et al. [1] described the different behaviors of Vδ1pos and Vδ2pos T cell subsets in response to lifelong stress and claimed that Vδ2pos T cells are not affected by aging and Human Cytomegalovirus (HCMV) infection. While we agree that these two γδ T cell subsets diverge both in phenotype/function and in tissue distribution, we are somewhat surprised that authors did not take into account the several previously published and contradictory experimental evidence in regards to senescence of Vδ2pos T cells [2,3]. These latter studies reported that HCMV infection not only induces a clonal expansion of a distinct Vγ9neg/Vδ2pos T cell subset, but also determines a concomitant adaptive differentiation from CD27high naïve cells to CD27low/neg terminal-effectors. However, Weili Xu et al. argued that the expression and kinetics of both CD27 and CD45RA surface markers do not change and follow the homeostatic changes of Vδ2pos T cells. This statement goes in the opposite direction to previously reported findings as the CD27/CD45RA phenotype has been shown to mark the maturation and differentiation (TNaïve, TCentral-Memory, Teffector-Memory and TEffectory-Memory RA) of Vδ2pos T cells. Indeed, the different surface expression of both CD27 and CD45 parallel the progressive decrease of telomere length, the proliferative capacity as well as the different effector-functions and resistance to death of Vδ2+ T cells in response to antigens and homeostatic cytokines [4,5]. Hence, we believe that these controversial issues require further discussion beyond the unilateral conclusion given by the study of Weili Xu et al.