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The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells

Natural killer (NK) cells and dendritic cells (DC) are thought to play critical roles in the first phases of HIV infection. In this study, we examined changes in the NK cell repertoire and functions occurring in response to early interaction with HIV-infected DC, using an autologous in vitro NK/DC c...

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Autores principales: Scott-Algara, Daniel, Arnold, Vincent, Didier, Céline, Kattan, Tarek, Pirozzi, Gianluca, Barré-Sinoussi, Françoise, Pancino, Gianfranco
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2276866/
https://www.ncbi.nlm.nih.gov/pubmed/18398485
http://dx.doi.org/10.1371/journal.pone.0001975
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author Scott-Algara, Daniel
Arnold, Vincent
Didier, Céline
Kattan, Tarek
Pirozzi, Gianluca
Barré-Sinoussi, Françoise
Pancino, Gianfranco
author_facet Scott-Algara, Daniel
Arnold, Vincent
Didier, Céline
Kattan, Tarek
Pirozzi, Gianluca
Barré-Sinoussi, Françoise
Pancino, Gianfranco
author_sort Scott-Algara, Daniel
collection PubMed
description Natural killer (NK) cells and dendritic cells (DC) are thought to play critical roles in the first phases of HIV infection. In this study, we examined changes in the NK cell repertoire and functions occurring in response to early interaction with HIV-infected DC, using an autologous in vitro NK/DC coculture system. We show that NK cell interaction with HIV-1-infected autologous monocyte-derived DC (MDDC) modulates NK receptor expression. In particular, expression of the CD85j receptor on NK cells was strongly down-regulated upon coculture with HIV-1-infected MDDC. We demonstrate that CD85j(+) NK cells exert potent control of HIV-1 replication in single-round and productively HIV-1-infected MDDC, whereas CD85j(−) NK cells induce a modest and transient decrease of HIV-1 replication. HIV-1 suppression in MDCC by CD85j(+) NK cells required cell-to-cell contact and did not appear mediated by cytotoxicity or by soluble factors. HIV-1 inhibition was abolished when NK-MDDC interaction through the CD85j receptor was blocked with a recombinant CD85j molecule, whereas inhibition was only slightly counteracted by blocking HLA class I molecules, which are known CD85j ligands. After masking HLA class I molecules with specific antibodies, a fraction of HIV-1 infected MDDC was still strongly stained by a recombinant CD85j protein. These results suggest that CD85j(+) NK cell inhibition of HIV-1 replication in MDDC is mainly mediated by CD85j interaction with an unknown ligand (distinct from HLA class I molecules) preferentially expressed on HIV-1-infected MDDC.
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spelling pubmed-22768662008-04-09 The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells Scott-Algara, Daniel Arnold, Vincent Didier, Céline Kattan, Tarek Pirozzi, Gianluca Barré-Sinoussi, Françoise Pancino, Gianfranco PLoS One Research Article Natural killer (NK) cells and dendritic cells (DC) are thought to play critical roles in the first phases of HIV infection. In this study, we examined changes in the NK cell repertoire and functions occurring in response to early interaction with HIV-infected DC, using an autologous in vitro NK/DC coculture system. We show that NK cell interaction with HIV-1-infected autologous monocyte-derived DC (MDDC) modulates NK receptor expression. In particular, expression of the CD85j receptor on NK cells was strongly down-regulated upon coculture with HIV-1-infected MDDC. We demonstrate that CD85j(+) NK cells exert potent control of HIV-1 replication in single-round and productively HIV-1-infected MDDC, whereas CD85j(−) NK cells induce a modest and transient decrease of HIV-1 replication. HIV-1 suppression in MDCC by CD85j(+) NK cells required cell-to-cell contact and did not appear mediated by cytotoxicity or by soluble factors. HIV-1 inhibition was abolished when NK-MDDC interaction through the CD85j receptor was blocked with a recombinant CD85j molecule, whereas inhibition was only slightly counteracted by blocking HLA class I molecules, which are known CD85j ligands. After masking HLA class I molecules with specific antibodies, a fraction of HIV-1 infected MDDC was still strongly stained by a recombinant CD85j protein. These results suggest that CD85j(+) NK cell inhibition of HIV-1 replication in MDDC is mainly mediated by CD85j interaction with an unknown ligand (distinct from HLA class I molecules) preferentially expressed on HIV-1-infected MDDC. Public Library of Science 2008-04-09 /pmc/articles/PMC2276866/ /pubmed/18398485 http://dx.doi.org/10.1371/journal.pone.0001975 Text en Scott-Algara et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Scott-Algara, Daniel
Arnold, Vincent
Didier, Céline
Kattan, Tarek
Pirozzi, Gianluca
Barré-Sinoussi, Françoise
Pancino, Gianfranco
The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells
title The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells
title_full The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells
title_fullStr The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells
title_full_unstemmed The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells
title_short The CD85j(+) NK Cell Subset Potently Controls HIV-1 Replication in Autologous Dendritic Cells
title_sort cd85j(+) nk cell subset potently controls hiv-1 replication in autologous dendritic cells
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2276866/
https://www.ncbi.nlm.nih.gov/pubmed/18398485
http://dx.doi.org/10.1371/journal.pone.0001975
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