HIV Infection of Monocytes-Derived Dendritic Cells Inhibits Vc9Vd2 T Cells Functions

DCs act as sentinel cells against incoming pathogens and represent the most potent antigen presenting cells, having the unique capability to prime naı̈ve T cells. In addition to their role in induction of adaptive immune responses, DC are also able to activate innate cells as cd T cells; in particular, a reciprocal crosstalk between DC and cd T cells was demonstrated. However, whether HIV infection may alter DC-Vc9Vd2 T cells cross-talk was not yet described. To clarify this issue, we cultured activated Vc9Vd2 T cells with HIV infected monocyte derived DC (MoDC). After 5 days we evaluated MoDC phenotype, and Vc9Vd2 T cells activation and proliferation. In our model, Vc9Vd2 T cells were not able to proliferate in response to HIV-infected MoDC, although an up-regulation of CD69 was observed. Upon phosphoantigens stimulation, Vc9Vd2 T cells proliferation and cytokine production were inhibited when cultured with HIV-infected MoDC in a cell-contact dependent way. Moreover, HIV-infected MoDC are not able to up-regulate CD86 molecules when cultured with activated Vc9Vd2 T cells, compared with uninfected MoDC. Further, activated Vc9Vd2 T cells are not able to induce HLA DR up-regulation and CCR5 down-regulation on HIV-infected MoDC. These data indicate that HIV-infected DC alter the capacity of Vc9Vd2 T cells to respond to their antigens, pointing out a new mechanisms of induction of Vc9Vd2 T cells anergy carried out by HIV, that could contribute to immune evasion