HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 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 naïve 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 particula...
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doaj-6162b000b22749ae8fc1970211ab38492020-11-25T01:32:03ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-01910e11109510.1371/journal.pone.0111095HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 T cells functions.Alessandra SacchiAlessandra RinaldiNicola TuminoRita CasettiChiara AgratiFederica TurchiVeronica BordoniEleonora CiminiFederico MartiniDCs act as sentinel cells against incoming pathogens and represent the most potent antigen presenting cells, having the unique capability to prime naïve 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.http://europepmc.org/articles/PMC4207784?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Alessandra Sacchi Alessandra Rinaldi Nicola Tumino Rita Casetti Chiara Agrati Federica Turchi Veronica Bordoni Eleonora Cimini Federico Martini |
spellingShingle |
Alessandra Sacchi Alessandra Rinaldi Nicola Tumino Rita Casetti Chiara Agrati Federica Turchi Veronica Bordoni Eleonora Cimini Federico Martini HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 T cells functions. PLoS ONE |
author_facet |
Alessandra Sacchi Alessandra Rinaldi Nicola Tumino Rita Casetti Chiara Agrati Federica Turchi Veronica Bordoni Eleonora Cimini Federico Martini |
author_sort |
Alessandra Sacchi |
title |
HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 T cells functions. |
title_short |
HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 T cells functions. |
title_full |
HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 T cells functions. |
title_fullStr |
HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 T cells functions. |
title_full_unstemmed |
HIV infection of monocytes-derived dendritic cells inhibits Vγ9Vδ2 T cells functions. |
title_sort |
hiv infection of monocytes-derived dendritic cells inhibits vγ9vδ2 t cells functions. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2014-01-01 |
description |
DCs act as sentinel cells against incoming pathogens and represent the most potent antigen presenting cells, having the unique capability to prime naïve 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. |
url |
http://europepmc.org/articles/PMC4207784?pdf=render |
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