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Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1

Standard

Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1. / Garcia-Beltran, Wilfredo F; Hölzemer, Angelique; Martrus, Gloria; Chung, Amy W; Pacheco, Yovana; Simoneau, Camille R; Rucevic, Marijana; Lamothe-Molina, Pedro A; Pertel, Thomas; Kim, Tae-Eun; Dugan, Haley; Alter, Galit; Dechanet-Merville, Julie; Jost, Stephanie; Carrington, Mary; Altfeld, Marcus.

in: NAT IMMUNOL, Jahrgang 17, Nr. 9, 09.2016, S. 1067-74.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Garcia-Beltran, WF, Hölzemer, A, Martrus, G, Chung, AW, Pacheco, Y, Simoneau, CR, Rucevic, M, Lamothe-Molina, PA, Pertel, T, Kim, T-E, Dugan, H, Alter, G, Dechanet-Merville, J, Jost, S, Carrington, M & Altfeld, M 2016, 'Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1', NAT IMMUNOL, Jg. 17, Nr. 9, S. 1067-74. https://doi.org/10.1038/ni.3513

APA

Garcia-Beltran, W. F., Hölzemer, A., Martrus, G., Chung, A. W., Pacheco, Y., Simoneau, C. R., Rucevic, M., Lamothe-Molina, P. A., Pertel, T., Kim, T-E., Dugan, H., Alter, G., Dechanet-Merville, J., Jost, S., Carrington, M., & Altfeld, M. (2016). Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1. NAT IMMUNOL, 17(9), 1067-74. https://doi.org/10.1038/ni.3513

Vancouver

Garcia-Beltran WF, Hölzemer A, Martrus G, Chung AW, Pacheco Y, Simoneau CR et al. Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1. NAT IMMUNOL. 2016 Sep;17(9):1067-74. https://doi.org/10.1038/ni.3513

Bibtex

@article{4601793be274496090f3a66a8412fbfc,
title = "Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1",
abstract = "The activating natural killer (NK)-cell receptor KIR3DS1 has been linked to the outcome of various human diseases, including delayed progression of disease caused by human immunodeficiency virus type 1 (HIV-1), yet a ligand that would account for its biological effects has remained unknown. We screened 100 HLA class I proteins and found that KIR3DS1 bound to HLA-F, a result we confirmed biochemically and functionally. Primary human KIR3DS1(+) NK cells degranulated and produced antiviral cytokines after encountering HLA-F and inhibited HIV-1 replication in vitro. Activation of CD4(+) T cells triggered the transcription and surface expression of HLA-F mRNA and HLA-F protein, respectively, and induced binding of KIR3DS1. HIV-1 infection further increased the transcription of HLA-F mRNA but decreased the binding of KIR3DS1, indicative of a mechanism for evading recognition by KIR3DS1(+) NK cells. Thus, we have established HLA-F as a ligand of KIR3DS1 and have demonstrated cell-context-dependent expression of HLA-F that might explain the widespread influence of KIR3DS1 in human disease.",
keywords = "Journal Article",
author = "Garcia-Beltran, {Wilfredo F} and Angelique H{\"o}lzemer and Gloria Martrus and Chung, {Amy W} and Yovana Pacheco and Simoneau, {Camille R} and Marijana Rucevic and Lamothe-Molina, {Pedro A} and Thomas Pertel and Tae-Eun Kim and Haley Dugan and Galit Alter and Julie Dechanet-Merville and Stephanie Jost and Mary Carrington and Marcus Altfeld",
year = "2016",
month = sep,
doi = "10.1038/ni.3513",
language = "English",
volume = "17",
pages = "1067--74",
journal = "NAT IMMUNOL",
issn = "1529-2908",
publisher = "NATURE PUBLISHING GROUP",
number = "9",

}

RIS

TY - JOUR

T1 - Open conformers of HLA-F are high-affinity ligands of the activating NK-cell receptor KIR3DS1

AU - Garcia-Beltran, Wilfredo F

AU - Hölzemer, Angelique

AU - Martrus, Gloria

AU - Chung, Amy W

AU - Pacheco, Yovana

AU - Simoneau, Camille R

AU - Rucevic, Marijana

AU - Lamothe-Molina, Pedro A

AU - Pertel, Thomas

AU - Kim, Tae-Eun

AU - Dugan, Haley

AU - Alter, Galit

AU - Dechanet-Merville, Julie

AU - Jost, Stephanie

AU - Carrington, Mary

AU - Altfeld, Marcus

PY - 2016/9

Y1 - 2016/9

N2 - The activating natural killer (NK)-cell receptor KIR3DS1 has been linked to the outcome of various human diseases, including delayed progression of disease caused by human immunodeficiency virus type 1 (HIV-1), yet a ligand that would account for its biological effects has remained unknown. We screened 100 HLA class I proteins and found that KIR3DS1 bound to HLA-F, a result we confirmed biochemically and functionally. Primary human KIR3DS1(+) NK cells degranulated and produced antiviral cytokines after encountering HLA-F and inhibited HIV-1 replication in vitro. Activation of CD4(+) T cells triggered the transcription and surface expression of HLA-F mRNA and HLA-F protein, respectively, and induced binding of KIR3DS1. HIV-1 infection further increased the transcription of HLA-F mRNA but decreased the binding of KIR3DS1, indicative of a mechanism for evading recognition by KIR3DS1(+) NK cells. Thus, we have established HLA-F as a ligand of KIR3DS1 and have demonstrated cell-context-dependent expression of HLA-F that might explain the widespread influence of KIR3DS1 in human disease.

AB - The activating natural killer (NK)-cell receptor KIR3DS1 has been linked to the outcome of various human diseases, including delayed progression of disease caused by human immunodeficiency virus type 1 (HIV-1), yet a ligand that would account for its biological effects has remained unknown. We screened 100 HLA class I proteins and found that KIR3DS1 bound to HLA-F, a result we confirmed biochemically and functionally. Primary human KIR3DS1(+) NK cells degranulated and produced antiviral cytokines after encountering HLA-F and inhibited HIV-1 replication in vitro. Activation of CD4(+) T cells triggered the transcription and surface expression of HLA-F mRNA and HLA-F protein, respectively, and induced binding of KIR3DS1. HIV-1 infection further increased the transcription of HLA-F mRNA but decreased the binding of KIR3DS1, indicative of a mechanism for evading recognition by KIR3DS1(+) NK cells. Thus, we have established HLA-F as a ligand of KIR3DS1 and have demonstrated cell-context-dependent expression of HLA-F that might explain the widespread influence of KIR3DS1 in human disease.

KW - Journal Article

U2 - 10.1038/ni.3513

DO - 10.1038/ni.3513

M3 - SCORING: Journal article

C2 - 27455421

VL - 17

SP - 1067

EP - 1074

JO - NAT IMMUNOL

JF - NAT IMMUNOL

SN - 1529-2908

IS - 9

ER -