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HLA class I signal peptide polymorphism determines the level of CD94/NKG2-HLA-E-mediated regulation of effector cell responses

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HLA class I signal peptide polymorphism determines the level of CD94/NKG2-HLA-E-mediated regulation of effector cell responses. / Lin, Zhansong; Bashirova, Arman A; Viard, Mathias; Garner, Lee; Quastel, Max; Beiersdorfer, Maya; Kasprzak, Wojciech K; Akdag, Marjan; Yuki, Yuko; Ojeda, Pedro; Das, Sudipto; Andresson, Thorkell; Naranbhai, Vivek; Horowitz, Amir; McMichael, Andrew J; Hoelzemer, Angelique; Gillespie, Geraldine M; Garcia-Beltran, Wilfredo F; Carrington, Mary.

In: NAT IMMUNOL, Vol. 24, No. 7, 06.2023, p. 1087-1097.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Lin, Z, Bashirova, AA, Viard, M, Garner, L, Quastel, M, Beiersdorfer, M, Kasprzak, WK, Akdag, M, Yuki, Y, Ojeda, P, Das, S, Andresson, T, Naranbhai, V, Horowitz, A, McMichael, AJ, Hoelzemer, A, Gillespie, GM, Garcia-Beltran, WF & Carrington, M 2023, 'HLA class I signal peptide polymorphism determines the level of CD94/NKG2-HLA-E-mediated regulation of effector cell responses', NAT IMMUNOL, vol. 24, no. 7, pp. 1087-1097. https://doi.org/10.1038/s41590-023-01523-z

APA

Lin, Z., Bashirova, A. A., Viard, M., Garner, L., Quastel, M., Beiersdorfer, M., Kasprzak, W. K., Akdag, M., Yuki, Y., Ojeda, P., Das, S., Andresson, T., Naranbhai, V., Horowitz, A., McMichael, A. J., Hoelzemer, A., Gillespie, G. M., Garcia-Beltran, W. F., & Carrington, M. (2023). HLA class I signal peptide polymorphism determines the level of CD94/NKG2-HLA-E-mediated regulation of effector cell responses. NAT IMMUNOL, 24(7), 1087-1097. https://doi.org/10.1038/s41590-023-01523-z

Vancouver

Lin Z, Bashirova AA, Viard M, Garner L, Quastel M, Beiersdorfer M et al. HLA class I signal peptide polymorphism determines the level of CD94/NKG2-HLA-E-mediated regulation of effector cell responses. NAT IMMUNOL. 2023 Jun;24(7):1087-1097. https://doi.org/10.1038/s41590-023-01523-z

Bibtex

@article{30fe18f7c6b94844b2dbbdcfe3948031,
title = "HLA class I signal peptide polymorphism determines the level of CD94/NKG2-HLA-E-mediated regulation of effector cell responses",
abstract = "Human leukocyte antigen (HLA)-E binds epitopes derived from HLA-A, HLA-B, HLA-C and HLA-G signal peptides (SPs) and serves as a ligand for CD94/NKG2A and CD94/NKG2C receptors expressed on natural killer and T cell subsets. We show that among 16 common classical HLA class I SP variants, only 6 can be efficiently processed to generate epitopes that enable CD94/NKG2 engagement, which we term 'functional SPs'. The single functional HLA-B SP, known as HLA-B/-21M, induced high HLA-E expression, but conferred the lowest receptor recognition. Consequently, HLA-B/-21M SP competes with other SPs for providing epitope to HLA-E and reduces overall recognition of target cells by CD94/NKG2A, calling for reassessment of previous disease models involving HLA-B/-21M. Genetic population data indicate a positive correlation between frequencies of functional SPs in humans and corresponding cytomegalovirus mimics, suggesting a means for viral escape from host responses. The systematic, quantitative approach described herein will facilitate development of prediction algorithms for accurately measuring the impact of CD94/NKG2-HLA-E interactions in disease resistance/susceptibility.",
keywords = "Humans, Protein Sorting Signals, Killer Cells, Natural, Histocompatibility Antigens Class I, HLA Antigens/metabolism, Histocompatibility Antigens Class II/metabolism, NK Cell Lectin-Like Receptor Subfamily D/genetics, Lectins, C-Type/metabolism, Receptors, Natural Killer Cell/metabolism, HLA-E Antigens",
author = "Zhansong Lin and Bashirova, {Arman A} and Mathias Viard and Lee Garner and Max Quastel and Maya Beiersdorfer and Kasprzak, {Wojciech K} and Marjan Akdag and Yuko Yuki and Pedro Ojeda and Sudipto Das and Thorkell Andresson and Vivek Naranbhai and Amir Horowitz and McMichael, {Andrew J} and Angelique Hoelzemer and Gillespie, {Geraldine M} and Garcia-Beltran, {Wilfredo F} and Mary Carrington",
note = "{\textcopyright} 2023. The Author(s), under exclusive licence to Springer Nature America, Inc.",
year = "2023",
month = jun,
doi = "10.1038/s41590-023-01523-z",
language = "English",
volume = "24",
pages = "1087--1097",
journal = "NAT IMMUNOL",
issn = "1529-2908",
publisher = "NATURE PUBLISHING GROUP",
number = "7",

}

RIS

TY - JOUR

T1 - HLA class I signal peptide polymorphism determines the level of CD94/NKG2-HLA-E-mediated regulation of effector cell responses

AU - Lin, Zhansong

AU - Bashirova, Arman A

AU - Viard, Mathias

AU - Garner, Lee

AU - Quastel, Max

AU - Beiersdorfer, Maya

AU - Kasprzak, Wojciech K

AU - Akdag, Marjan

AU - Yuki, Yuko

AU - Ojeda, Pedro

AU - Das, Sudipto

AU - Andresson, Thorkell

AU - Naranbhai, Vivek

AU - Horowitz, Amir

AU - McMichael, Andrew J

AU - Hoelzemer, Angelique

AU - Gillespie, Geraldine M

AU - Garcia-Beltran, Wilfredo F

AU - Carrington, Mary

N1 - © 2023. The Author(s), under exclusive licence to Springer Nature America, Inc.

PY - 2023/6

Y1 - 2023/6

N2 - Human leukocyte antigen (HLA)-E binds epitopes derived from HLA-A, HLA-B, HLA-C and HLA-G signal peptides (SPs) and serves as a ligand for CD94/NKG2A and CD94/NKG2C receptors expressed on natural killer and T cell subsets. We show that among 16 common classical HLA class I SP variants, only 6 can be efficiently processed to generate epitopes that enable CD94/NKG2 engagement, which we term 'functional SPs'. The single functional HLA-B SP, known as HLA-B/-21M, induced high HLA-E expression, but conferred the lowest receptor recognition. Consequently, HLA-B/-21M SP competes with other SPs for providing epitope to HLA-E and reduces overall recognition of target cells by CD94/NKG2A, calling for reassessment of previous disease models involving HLA-B/-21M. Genetic population data indicate a positive correlation between frequencies of functional SPs in humans and corresponding cytomegalovirus mimics, suggesting a means for viral escape from host responses. The systematic, quantitative approach described herein will facilitate development of prediction algorithms for accurately measuring the impact of CD94/NKG2-HLA-E interactions in disease resistance/susceptibility.

AB - Human leukocyte antigen (HLA)-E binds epitopes derived from HLA-A, HLA-B, HLA-C and HLA-G signal peptides (SPs) and serves as a ligand for CD94/NKG2A and CD94/NKG2C receptors expressed on natural killer and T cell subsets. We show that among 16 common classical HLA class I SP variants, only 6 can be efficiently processed to generate epitopes that enable CD94/NKG2 engagement, which we term 'functional SPs'. The single functional HLA-B SP, known as HLA-B/-21M, induced high HLA-E expression, but conferred the lowest receptor recognition. Consequently, HLA-B/-21M SP competes with other SPs for providing epitope to HLA-E and reduces overall recognition of target cells by CD94/NKG2A, calling for reassessment of previous disease models involving HLA-B/-21M. Genetic population data indicate a positive correlation between frequencies of functional SPs in humans and corresponding cytomegalovirus mimics, suggesting a means for viral escape from host responses. The systematic, quantitative approach described herein will facilitate development of prediction algorithms for accurately measuring the impact of CD94/NKG2-HLA-E interactions in disease resistance/susceptibility.

KW - Humans

KW - Protein Sorting Signals

KW - Killer Cells, Natural

KW - Histocompatibility Antigens Class I

KW - HLA Antigens/metabolism

KW - Histocompatibility Antigens Class II/metabolism

KW - NK Cell Lectin-Like Receptor Subfamily D/genetics

KW - Lectins, C-Type/metabolism

KW - Receptors, Natural Killer Cell/metabolism

KW - HLA-E Antigens

U2 - 10.1038/s41590-023-01523-z

DO - 10.1038/s41590-023-01523-z

M3 - SCORING: Journal article

C2 - 37264229

VL - 24

SP - 1087

EP - 1097

JO - NAT IMMUNOL

JF - NAT IMMUNOL

SN - 1529-2908

IS - 7

ER -