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Scientific paper - Original scientific paper
Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection
The Journal of Immunology, 199 (2017), 5; 1567-1571. https://doi.org/10.4049/jimmunol.1700799
Nabekura, Tsukasa; Gotthardt, Dagmar; Niizuma, Kouta; Tršan, Tihana; Jenuš, Tina; Jonjić, Stipan; Lanier, Lewis L.

Institutional repository: Repository of the University of Rijeka, Faculty of Medicine

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Nabekura, T., Gotthardt, D., Niizuma, K., Tršan, T., Jenuš, T., Jonjić, S. & Lanier, L. L. (2017). Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection. The Journal of Immunology, 199. (5), 1567-1571. doi: 10.4049/jimmunol.1700799

Nabekura, Tsukasa, et al. "Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection." The Journal of Immunology, vol. 199, no. 5, 2017, pp. 1567-1571. https://doi.org/10.4049/jimmunol.1700799

Nabekura, Tsukasa, Dagmar Gotthardt, Kouta Niizuma, Tihana Tršan, Tina Jenuš, Stipan Jonjić and Lewis L. Lanier. "Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection." The Journal of Immunology 199, no. 5 (2017): 1567-1571. https://doi.org/10.4049/jimmunol.1700799

Nabekura, T., et al. (2017) 'Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection', The Journal of Immunology, 199(5), pp. 1567-1571. doi: 10.4049/jimmunol.1700799

Nabekura T, Gotthardt D, Niizuma K, Tršan T, Jenuš T, Jonjić S, and sur.. Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection. The Journal of Immunology [Internet]. 2017 September 01 [cited 2024 May 14];199(5):1567-1571. doi: 10.4049/jimmunol.1700799

T. Nabekura, et al., "Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection", The Journal of Immunology, vol. 199, no. 5, pp. 1567-1571, September 2017. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:981243. [Accessed: 14 May 2024]

Metadata
Title (english)Cutting Edge: NKG2D Signaling Enhances NK Cell Responses but Alone Is Insufficient To Drive Expansion during Mouse Cytomegalovirus Infection
AuthorTsukasa Nabekura
AuthorDagmar Gotthardt
AuthorKouta Niizuma
AuthorTihana Tršan
AuthorTina Jenuš
AuthorStipan Jonjić
AuthorLewis L. Lanier
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Histology and Embryology)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
NK cells play a critical role in host defense against viruses. In this study, we investigated the role of NKG2D in the expansion of NK cells after mouse CMV (MCMV) infection. Wild-type and NKG2D-deficient (Klrk1−/−) Ly49H+ NK cells proliferated robustly when infected with MCMV strains engineered to allow expression of NKG2D ligands, which enhanced the response of wild-type NK cells. Naive NK cells exclusively express NKG2D-L, which pairs only with DAP10, whereas NKG2D-S expressed by activated NK cells pairs with DAP10 and DAP12, similar to Ly49H. However, NKG2D alone was unable to drive robust expansion of Ly49H− NK cells when mice were infected with these MCMV strains, likely because NKG2D-S was only transiently expressed postinfection. These findings demonstrate that NKG2D augments Ly49H-dependent proliferation of NK cells; however, NKG2D signaling alone is inadequate for expansion of NK cells, likely due to only transient expression of the NKG2D–DAP12 complex.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleThe Journal of Immunology
Numberingvol. 199, no. 5, pp. 1567-1571
p-ISSN0022-1767
e-ISSN1550-6606
DOIhttps://doi.org/10.4049/jimmunol.1700799
URN:NBNurn:nbn:hr:184:981243
Publication2017-09-01
Publication2017-07-31
ProjectNumber: 322693
Title (croatian): Strengthening adaptive immunity via innate immunity: enhancing the CD8 T cell response by using the NKG2D ligand expressed in a herpesvirus vector
Acronym: STADVINN
Jurisdiction: eu
Funding stream: FP7
ProjectNumber: 062-0621261-1263
Title (croatian): Molekularni mehanizmi citomegalovirusnog izmicanja imunološkom nadzoru
Leader: Stipan Jonjić
Jurisdiction: Croatia
Funding stream: ZP
Document URLhttp://www.jimmunol.org/lookup/doi/10.4049/jimmunol.1700799
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) icon
Created on2018-10-30 20:45:26