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Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides
Dendritic cells (DCs) are essential antigen-presenting cells for the induction of immunity against pathogens. However, HIV-1 spread is strongly enhanced in clusters of DCs and CD4(+) T cells. Uninfected DCs capture HIV-1 and mediate viral transfer to bystander CD4(+) T cells through a process termed...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525531/ https://www.ncbi.nlm.nih.gov/pubmed/23271952 http://dx.doi.org/10.1371/journal.pbio.1001448 |
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author | Izquierdo-Useros, Nuria Lorizate, Maier Puertas, Maria C. Rodriguez-Plata, Maria T. Zangger, Nadine Erikson, Elina Pino, Maria Erkizia, Itziar Glass, Bärbel Clotet, Bonaventura Keppler, Oliver T. Telenti, Amalio Kräusslich, Hans-Georg Martinez-Picado, Javier |
author_facet | Izquierdo-Useros, Nuria Lorizate, Maier Puertas, Maria C. Rodriguez-Plata, Maria T. Zangger, Nadine Erikson, Elina Pino, Maria Erkizia, Itziar Glass, Bärbel Clotet, Bonaventura Keppler, Oliver T. Telenti, Amalio Kräusslich, Hans-Georg Martinez-Picado, Javier |
author_sort | Izquierdo-Useros, Nuria |
collection | PubMed |
description | Dendritic cells (DCs) are essential antigen-presenting cells for the induction of immunity against pathogens. However, HIV-1 spread is strongly enhanced in clusters of DCs and CD4(+) T cells. Uninfected DCs capture HIV-1 and mediate viral transfer to bystander CD4(+) T cells through a process termed trans-infection. Initial studies identified the C-type lectin DC-SIGN as the HIV-1 binding factor on DCs, which interacts with the viral envelope glycoproteins. Upon DC maturation, however, DC-SIGN is down-regulated, while HIV-1 capture and trans-infection is strongly enhanced via a glycoprotein-independent capture pathway that recognizes sialyllactose-containing membrane gangliosides. Here we show that the sialic acid-binding Ig-like lectin 1 (Siglec-1, CD169), which is highly expressed on mature DCs, specifically binds HIV-1 and vesicles carrying sialyllactose. Furthermore, Siglec-1 is essential for trans-infection by mature DCs. These findings identify Siglec-1 as a key factor for HIV-1 spread via infectious DC/T-cell synapses, highlighting a novel mechanism that mediates HIV-1 dissemination in activated tissues. |
format | Online Article Text |
id | pubmed-3525531 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-35255312012-12-27 Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides Izquierdo-Useros, Nuria Lorizate, Maier Puertas, Maria C. Rodriguez-Plata, Maria T. Zangger, Nadine Erikson, Elina Pino, Maria Erkizia, Itziar Glass, Bärbel Clotet, Bonaventura Keppler, Oliver T. Telenti, Amalio Kräusslich, Hans-Georg Martinez-Picado, Javier PLoS Biol Research Article Dendritic cells (DCs) are essential antigen-presenting cells for the induction of immunity against pathogens. However, HIV-1 spread is strongly enhanced in clusters of DCs and CD4(+) T cells. Uninfected DCs capture HIV-1 and mediate viral transfer to bystander CD4(+) T cells through a process termed trans-infection. Initial studies identified the C-type lectin DC-SIGN as the HIV-1 binding factor on DCs, which interacts with the viral envelope glycoproteins. Upon DC maturation, however, DC-SIGN is down-regulated, while HIV-1 capture and trans-infection is strongly enhanced via a glycoprotein-independent capture pathway that recognizes sialyllactose-containing membrane gangliosides. Here we show that the sialic acid-binding Ig-like lectin 1 (Siglec-1, CD169), which is highly expressed on mature DCs, specifically binds HIV-1 and vesicles carrying sialyllactose. Furthermore, Siglec-1 is essential for trans-infection by mature DCs. These findings identify Siglec-1 as a key factor for HIV-1 spread via infectious DC/T-cell synapses, highlighting a novel mechanism that mediates HIV-1 dissemination in activated tissues. Public Library of Science 2012-12-18 /pmc/articles/PMC3525531/ /pubmed/23271952 http://dx.doi.org/10.1371/journal.pbio.1001448 Text en © 2012 Izquierdo-Useros 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 Izquierdo-Useros, Nuria Lorizate, Maier Puertas, Maria C. Rodriguez-Plata, Maria T. Zangger, Nadine Erikson, Elina Pino, Maria Erkizia, Itziar Glass, Bärbel Clotet, Bonaventura Keppler, Oliver T. Telenti, Amalio Kräusslich, Hans-Georg Martinez-Picado, Javier Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides |
title | Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides |
title_full | Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides |
title_fullStr | Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides |
title_full_unstemmed | Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides |
title_short | Siglec-1 Is a Novel Dendritic Cell Receptor That Mediates HIV-1 Trans-Infection Through Recognition of Viral Membrane Gangliosides |
title_sort | siglec-1 is a novel dendritic cell receptor that mediates hiv-1 trans-infection through recognition of viral membrane gangliosides |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3525531/ https://www.ncbi.nlm.nih.gov/pubmed/23271952 http://dx.doi.org/10.1371/journal.pbio.1001448 |
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