Characterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.

Human natural killer (NK) cell differentiation, characterized by a loss of NKG2A in parallel with the acquisition of NKG2C, KIRs, and CD57 is stimulated by a number of virus infections, including infection with human cytomegalovirus (CMV), hantavirus, chikungunya virus, and HIV-1. Here, we addressed...

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Autores principales: Niklas K Björkström, Alexandra Svensson, Karl-Johan Malmberg, Kristina Eriksson, Hans-Gustaf Ljunggren
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Publicado: Public Library of Science (PLoS) 2011
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Acceso en línea:https://doaj.org/article/6bcb313599a5494c8b90014013de4f74
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spelling oai:doaj.org-article:6bcb313599a5494c8b90014013de4f742021-11-18T07:34:17ZCharacterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.1932-620310.1371/journal.pone.0027664https://doaj.org/article/6bcb313599a5494c8b90014013de4f742011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22110712/?tool=EBIhttps://doaj.org/toc/1932-6203Human natural killer (NK) cell differentiation, characterized by a loss of NKG2A in parallel with the acquisition of NKG2C, KIRs, and CD57 is stimulated by a number of virus infections, including infection with human cytomegalovirus (CMV), hantavirus, chikungunya virus, and HIV-1. Here, we addressed if HSV-2 infection in a similar way drives NK cell differentiation towards an NKG2A(-)NKG2C(+)KIR(+)CD57(+) phenotype. In contrast to infection with CMV, hantavirus, chikungunya virus, and HIV-1, recurrent HSV-2 infection did not yield an accumulation of highly differentiated NK cells in human peripheral blood. This outcome indicates that human HSV-2 infection has no significant imprinting effect on the human NK cell repertoire.Niklas K BjörkströmAlexandra SvenssonKarl-Johan MalmbergKristina ErikssonHans-Gustaf LjunggrenPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 11, p e27664 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Niklas K Björkström
Alexandra Svensson
Karl-Johan Malmberg
Kristina Eriksson
Hans-Gustaf Ljunggren
Characterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.
description Human natural killer (NK) cell differentiation, characterized by a loss of NKG2A in parallel with the acquisition of NKG2C, KIRs, and CD57 is stimulated by a number of virus infections, including infection with human cytomegalovirus (CMV), hantavirus, chikungunya virus, and HIV-1. Here, we addressed if HSV-2 infection in a similar way drives NK cell differentiation towards an NKG2A(-)NKG2C(+)KIR(+)CD57(+) phenotype. In contrast to infection with CMV, hantavirus, chikungunya virus, and HIV-1, recurrent HSV-2 infection did not yield an accumulation of highly differentiated NK cells in human peripheral blood. This outcome indicates that human HSV-2 infection has no significant imprinting effect on the human NK cell repertoire.
format article
author Niklas K Björkström
Alexandra Svensson
Karl-Johan Malmberg
Kristina Eriksson
Hans-Gustaf Ljunggren
author_facet Niklas K Björkström
Alexandra Svensson
Karl-Johan Malmberg
Kristina Eriksson
Hans-Gustaf Ljunggren
author_sort Niklas K Björkström
title Characterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.
title_short Characterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.
title_full Characterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.
title_fullStr Characterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.
title_full_unstemmed Characterization of natural killer cell phenotype and function during recurrent human HSV-2 infection.
title_sort characterization of natural killer cell phenotype and function during recurrent human hsv-2 infection.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/6bcb313599a5494c8b90014013de4f74
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