HIV infection of monocytes-derived dendritic cells inhibits Vc9Vd2 T cells functions

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Abstract

DCs act as sentinel cells against incoming pathogens and represent the most potent antigen presenting cells, having the unique capability to prime näive T cells. In addition to their role in induction of adaptive immune responses, DC are also able to activate innate cells as γδ T cells; in particular, a reciprocal crosstalk between DC and γδ T cells was demonstrated. However, whether HIV infection may alter DC-Vγ9Vδ2 T cells cross-talk was not yet described. To clarify this issue, we cultured activated Vγ9Vδ2 T cells with HIV infected monocyte derived DC (MoDC). After 5 days we evaluated MoDC phenotype, and Vγ9Vδ2 T cells activation and proliferation. In our model, Vγ9Vδ2 T cells were not able to proliferate in response to HIV-infected MoDC, although an up-regulation of CD69 was observed. Upon phosphoantigens stimulation, Vγ9Vδ2 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 Vγ9Vδ2 T cells, compared with uninfected MoDC. Further, activated Vγ9Vδ2 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 Vγ9Vδ2 T cells to respond to their antigens, pointing out a new mechanisms of induction of Vγ9Vδ2 T cells anergy carried out by HIV, that could contribute to immune evasion.

Original languageEnglish
Article number0111095
JournalPLoS One
Volume9
Issue number10
DOIs
Publication statusPublished - Oct 23 2014

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T-cells
HIV infections
dendritic cells
monocytes
Dendritic Cells
HIV Infections
Monocytes
T-lymphocytes
T-Lymphocytes
HIV
Up-Regulation
Cell Proliferation
immune evasion
Immune Evasion
antigen-presenting cells
Cell proliferation
Adaptive Immunity
HLA-DR Antigens
Pathogens
Antigen-Presenting Cells

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

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title = "HIV infection of monocytes-derived dendritic cells inhibits Vc9Vd2 T cells functions",
abstract = "DCs act as sentinel cells against incoming pathogens and represent the most potent antigen presenting cells, having the unique capability to prime n{\"a}ive T cells. In addition to their role in induction of adaptive immune responses, DC are also able to activate innate cells as γδ T cells; in particular, a reciprocal crosstalk between DC and γδ T cells was demonstrated. However, whether HIV infection may alter DC-Vγ9Vδ2 T cells cross-talk was not yet described. To clarify this issue, we cultured activated Vγ9Vδ2 T cells with HIV infected monocyte derived DC (MoDC). After 5 days we evaluated MoDC phenotype, and Vγ9Vδ2 T cells activation and proliferation. In our model, Vγ9Vδ2 T cells were not able to proliferate in response to HIV-infected MoDC, although an up-regulation of CD69 was observed. Upon phosphoantigens stimulation, Vγ9Vδ2 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 Vγ9Vδ2 T cells, compared with uninfected MoDC. Further, activated Vγ9Vδ2 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 Vγ9Vδ2 T cells to respond to their antigens, pointing out a new mechanisms of induction of Vγ9Vδ2 T cells anergy carried out by HIV, that could contribute to immune evasion.",
author = "Alessandra Sacchi and Alessandra Rinaldi and Nicola Tumino and Rita Casetti and Chiara Agrati and Federica Turchi and Veronica Bordoni and Eleonora Cimini and Federico Martini",
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AU - Sacchi, Alessandra

AU - Rinaldi, Alessandra

AU - Tumino, Nicola

AU - Casetti, Rita

AU - Agrati, Chiara

AU - Turchi, Federica

AU - Bordoni, Veronica

AU - Cimini, Eleonora

AU - Martini, Federico

PY - 2014/10/23

Y1 - 2014/10/23

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