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.

Disclosure

Authors do not have any conflicts of interest to declare.