A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection

Abstract HIV infection affects 37 million people and about 1.7 million are infected annually. Among the phase III clinical trials only the RV144 vaccine trial elicited significant protection against HIV-1 acquisition, but the efficacy and immune memory were inadequate. To boost these vaccine functio...

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Autores principales:	Yufei Wang, Trevor Whittall, Stuart Neil, Gary Britton, Mukesh Mistry, Supachai Rerks-Ngarm, Punnee Pitisuttithum, Jaranit Kaewkungwal, Sorachai Nitayaphan, Xuesong Yu, Alicia Sato, Robert J. O’Connell, Nelson L. Michael, Merlin L. Robb, Jerome H. Kim, Thomas Lehner
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/fe03733a163a4761833618d8fb3d76d0
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spelling	oai:doaj.org-article:fe03733a163a4761833618d8fb3d76d02021-12-02T12:30:18ZA novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection10.1038/s41598-017-01188-32045-2322https://doaj.org/article/fe03733a163a4761833618d8fb3d76d02017-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01188-3https://doaj.org/toc/2045-2322Abstract HIV infection affects 37 million people and about 1.7 million are infected annually. Among the phase III clinical trials only the RV144 vaccine trial elicited significant protection against HIV-1 acquisition, but the efficacy and immune memory were inadequate. To boost these vaccine functions we studied T stem cell memory (TSCM) and innate immunity. TSCM cells were identified by phenotypic markers of CD4+ T cells and they were further characterised into 4 subsets. These expressed the common IL-2/IL-15 receptors and another subset of APOBEC3G anti-viral restriction factors, both of which were upregulated. In contrast, CD4+ TSCM cells expressing CCR5 co-receptors and α4β7 mucosal homing integrins were decreased. A parallel increase in CD4+ T cells was recorded with IL-15 receptors, APOBEC3G and CC chemokines, the latter downmodulating CCR5 molecules. We suggest a novel mechanism of dual memory stem cells; the established sequential memory pathway, TSCM →Central →Effector memory CD4+ T cells and the innate pathway consisting of the 4 subsets of TSCM. Both pathways are likely to be activated by endogenous HSP70. The TSCM memory stem cell and innate immunity pathways have to be optimised to boost the efficacy and immune memory of protection against HIV-1 in the clinical trial.Yufei WangTrevor WhittallStuart NeilGary BrittonMukesh MistrySupachai Rerks-NgarmPunnee PitisuttithumJaranit KaewkungwalSorachai NitayaphanXuesong YuAlicia SatoRobert J. O’ConnellNelson L. MichaelMerlin L. RobbJerome H. KimThomas LehnerNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yufei Wang Trevor Whittall Stuart Neil Gary Britton Mukesh Mistry Supachai Rerks-Ngarm Punnee Pitisuttithum Jaranit Kaewkungwal Sorachai Nitayaphan Xuesong Yu Alicia Sato Robert J. O’Connell Nelson L. Michael Merlin L. Robb Jerome H. Kim Thomas Lehner A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection
description	Abstract HIV infection affects 37 million people and about 1.7 million are infected annually. Among the phase III clinical trials only the RV144 vaccine trial elicited significant protection against HIV-1 acquisition, but the efficacy and immune memory were inadequate. To boost these vaccine functions we studied T stem cell memory (TSCM) and innate immunity. TSCM cells were identified by phenotypic markers of CD4+ T cells and they were further characterised into 4 subsets. These expressed the common IL-2/IL-15 receptors and another subset of APOBEC3G anti-viral restriction factors, both of which were upregulated. In contrast, CD4+ TSCM cells expressing CCR5 co-receptors and α4β7 mucosal homing integrins were decreased. A parallel increase in CD4+ T cells was recorded with IL-15 receptors, APOBEC3G and CC chemokines, the latter downmodulating CCR5 molecules. We suggest a novel mechanism of dual memory stem cells; the established sequential memory pathway, TSCM →Central →Effector memory CD4+ T cells and the innate pathway consisting of the 4 subsets of TSCM. Both pathways are likely to be activated by endogenous HSP70. The TSCM memory stem cell and innate immunity pathways have to be optimised to boost the efficacy and immune memory of protection against HIV-1 in the clinical trial.
format	article
author	Yufei Wang Trevor Whittall Stuart Neil Gary Britton Mukesh Mistry Supachai Rerks-Ngarm Punnee Pitisuttithum Jaranit Kaewkungwal Sorachai Nitayaphan Xuesong Yu Alicia Sato Robert J. O’Connell Nelson L. Michael Merlin L. Robb Jerome H. Kim Thomas Lehner
author_facet	Yufei Wang Trevor Whittall Stuart Neil Gary Britton Mukesh Mistry Supachai Rerks-Ngarm Punnee Pitisuttithum Jaranit Kaewkungwal Sorachai Nitayaphan Xuesong Yu Alicia Sato Robert J. O’Connell Nelson L. Michael Merlin L. Robb Jerome H. Kim Thomas Lehner
author_sort	Yufei Wang
title	A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection
title_short	A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection
title_full	A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection
title_fullStr	A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection
title_full_unstemmed	A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection
title_sort	novel mechanism linking memory stem cells with innate immunity in protection against hiv-1 infection
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/fe03733a163a4761833618d8fb3d76d0
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A novel mechanism linking memory stem cells with innate immunity in protection against HIV-1 infection

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