NK cell-like behavior of Valpha14i NK T cells during MCMV infection.

Immunity to the murine cytomegalovirus (MCMV) is critically dependent on the innate response for initial containment of viral replication, resolution of active infection, and proper induction of the adaptive phase of the anti-viral response. In contrast to NK cells, the Valpha14 invariant natural ki...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Johnna D Wesley, Marlowe S Tessmer, Deanna Chaukos, Laurent Brossay
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2008
Materias:
Acceso en línea:https://doaj.org/article/cf0c8f4b9ceb4e539891e22eb9329a32
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:cf0c8f4b9ceb4e539891e22eb9329a32
record_format dspace
spelling oai:doaj.org-article:cf0c8f4b9ceb4e539891e22eb9329a322021-11-25T05:46:30ZNK cell-like behavior of Valpha14i NK T cells during MCMV infection.1553-73661553-737410.1371/journal.ppat.1000106https://doaj.org/article/cf0c8f4b9ceb4e539891e22eb9329a322008-07-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18636102/pdf/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Immunity to the murine cytomegalovirus (MCMV) is critically dependent on the innate response for initial containment of viral replication, resolution of active infection, and proper induction of the adaptive phase of the anti-viral response. In contrast to NK cells, the Valpha14 invariant natural killer T cell response to MCMV has not been examined. We found that Valpha14i NK T cells become activated and produce significant levels of IFN-gamma, but do not proliferate or produce IL-4 following MCMV infection. In vivo treatment with an anti-CD1d mAb and adoptive transfer of Valpha14i NK T cells into MCMV-infected CD1d(-/-) mice demonstrate that CD1d is dispensable for Valpha14i NK T cell activation. In contrast, both IFN-alpha/beta and IL-12 are required for optimal activation. Valpha14i NK T cell-derived IFN-gamma is partially dependent on IFN-alpha/beta but highly dependent on IL-12. Valpha14i NK T cells contribute to the immune response to MCMV and amplify NK cell-derived IFN-gamma. Importantly, mortality is increased in CD1d(-/-) mice in response to high dose MCMV infection when compared to heterozygote littermate controls. Collectively, these findings illustrate the plasticity of Valpha14i NK T cells that act as effector T cells during bacterial infection, but have NK cell-like behavior during the innate immune response to MCMV infection.Johnna D WesleyMarlowe S TessmerDeanna ChaukosLaurent BrossayPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 4, Iss 7, p e1000106 (2008)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Johnna D Wesley
Marlowe S Tessmer
Deanna Chaukos
Laurent Brossay
NK cell-like behavior of Valpha14i NK T cells during MCMV infection.
description Immunity to the murine cytomegalovirus (MCMV) is critically dependent on the innate response for initial containment of viral replication, resolution of active infection, and proper induction of the adaptive phase of the anti-viral response. In contrast to NK cells, the Valpha14 invariant natural killer T cell response to MCMV has not been examined. We found that Valpha14i NK T cells become activated and produce significant levels of IFN-gamma, but do not proliferate or produce IL-4 following MCMV infection. In vivo treatment with an anti-CD1d mAb and adoptive transfer of Valpha14i NK T cells into MCMV-infected CD1d(-/-) mice demonstrate that CD1d is dispensable for Valpha14i NK T cell activation. In contrast, both IFN-alpha/beta and IL-12 are required for optimal activation. Valpha14i NK T cell-derived IFN-gamma is partially dependent on IFN-alpha/beta but highly dependent on IL-12. Valpha14i NK T cells contribute to the immune response to MCMV and amplify NK cell-derived IFN-gamma. Importantly, mortality is increased in CD1d(-/-) mice in response to high dose MCMV infection when compared to heterozygote littermate controls. Collectively, these findings illustrate the plasticity of Valpha14i NK T cells that act as effector T cells during bacterial infection, but have NK cell-like behavior during the innate immune response to MCMV infection.
format article
author Johnna D Wesley
Marlowe S Tessmer
Deanna Chaukos
Laurent Brossay
author_facet Johnna D Wesley
Marlowe S Tessmer
Deanna Chaukos
Laurent Brossay
author_sort Johnna D Wesley
title NK cell-like behavior of Valpha14i NK T cells during MCMV infection.
title_short NK cell-like behavior of Valpha14i NK T cells during MCMV infection.
title_full NK cell-like behavior of Valpha14i NK T cells during MCMV infection.
title_fullStr NK cell-like behavior of Valpha14i NK T cells during MCMV infection.
title_full_unstemmed NK cell-like behavior of Valpha14i NK T cells during MCMV infection.
title_sort nk cell-like behavior of valpha14i nk t cells during mcmv infection.
publisher Public Library of Science (PLoS)
publishDate 2008
url https://doaj.org/article/cf0c8f4b9ceb4e539891e22eb9329a32
work_keys_str_mv AT johnnadwesley nkcelllikebehaviorofvalpha14inktcellsduringmcmvinfection
AT marlowestessmer nkcelllikebehaviorofvalpha14inktcellsduringmcmvinfection
AT deannachaukos nkcelllikebehaviorofvalpha14inktcellsduringmcmvinfection
AT laurentbrossay nkcelllikebehaviorofvalpha14inktcellsduringmcmvinfection
_version_ 1718414486540386304