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Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway

Latent infection of primary CD34(+) progenitor cells by human cytomegalovirus (HCMV) results in their increased survival in the face of pro-apoptotic signals. For instance, we have shown previously that primary myeloid cells are refractory to FAS-mediated killing and that cellular IL-10 (cIL-10) is...

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Detalles Bibliográficos
Autores principales: Poole, Emma, Lau, Jonathan C. H., Sinclair, John
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Society for General Microbiology 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681070/
https://www.ncbi.nlm.nih.gov/pubmed/25957098
http://dx.doi.org/10.1099/vir.0.000180
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author Poole, Emma
Lau, Jonathan C. H.
Sinclair, John
author_facet Poole, Emma
Lau, Jonathan C. H.
Sinclair, John
author_sort Poole, Emma
collection PubMed
description Latent infection of primary CD34(+) progenitor cells by human cytomegalovirus (HCMV) results in their increased survival in the face of pro-apoptotic signals. For instance, we have shown previously that primary myeloid cells are refractory to FAS-mediated killing and that cellular IL-10 (cIL-10) is an important survival factor for this effect. However, how cIL-10 mediates this protection is unclear. Here, we have shown that cIL-10 signalling leading to upregulation of the cellular factor PEA-15 mediates latency-associated protection of CD34(+) progenitor cells from the extrinsic death pathway.
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spelling pubmed-46810702015-12-18 Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway Poole, Emma Lau, Jonathan C. H. Sinclair, John J Gen Virol Short Communication Latent infection of primary CD34(+) progenitor cells by human cytomegalovirus (HCMV) results in their increased survival in the face of pro-apoptotic signals. For instance, we have shown previously that primary myeloid cells are refractory to FAS-mediated killing and that cellular IL-10 (cIL-10) is an important survival factor for this effect. However, how cIL-10 mediates this protection is unclear. Here, we have shown that cIL-10 signalling leading to upregulation of the cellular factor PEA-15 mediates latency-associated protection of CD34(+) progenitor cells from the extrinsic death pathway. Society for General Microbiology 2015-08 /pmc/articles/PMC4681070/ /pubmed/25957098 http://dx.doi.org/10.1099/vir.0.000180 Text en © 2015 The Authors http://creativecommons.org/licenses/by/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/(.
spellingShingle Short Communication
Poole, Emma
Lau, Jonathan C. H.
Sinclair, John
Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway
title Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway
title_full Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway
title_fullStr Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway
title_full_unstemmed Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway
title_short Latent infection of myeloid progenitors by human cytomegalovirus protects cells from FAS-mediated apoptosis through the cellular IL-10/PEA-15 pathway
title_sort latent infection of myeloid progenitors by human cytomegalovirus protects cells from fas-mediated apoptosis through the cellular il-10/pea-15 pathway
topic Short Communication
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4681070/
https://www.ncbi.nlm.nih.gov/pubmed/25957098
http://dx.doi.org/10.1099/vir.0.000180
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