prikaz prve stranice dokumenta Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2
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Scientific paper - Original scientific paper
Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2
European Journal of Immunology, 50 (2020), 6; 880-890. https://doi.org/10.1002/eji.201948222
Prinz, Daniela; Klein, Klara; List, Julia; Knab, Vanessa M.; Menzl, Ingeborg; Leidenfrost, Nicoletta; Heller, Gerwin; Polić, Bojan; Putz, Eva Maria; Witalisz‐Siepracka, Agnieszka; Sexl, Veronika; Gotthardt, Dagmar

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Prinz, D., Klein, K., List, J., Knab, V. M., Menzl, I., Leidenfrost, N. ... Gotthardt, D. (2020). Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2. European Journal of Immunology, 50. (6), 880-890. doi: 10.1002/eji.201948222

Prinz, Daniela, et al. "Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2." European Journal of Immunology, vol. 50, no. 6, 2020, pp. 880-890. https://doi.org/10.1002/eji.201948222

Prinz, Daniela, Klara Klein, Julia List, Vanessa M. Knab, Ingeborg Menzl, Nicoletta Leidenfrost, Gerwin Heller, et al. "Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2." European Journal of Immunology 50, no. 6 (2020): 880-890. https://doi.org/10.1002/eji.201948222

Prinz, D., et al. (2020) 'Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2', European Journal of Immunology, 50(6), pp. 880-890. doi: 10.1002/eji.201948222

Prinz D, Klein K, List J, Knab VM, Menzl I, Leidenfrost N, and sur.. Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2. European Journal of Immunology [Internet]. 2020 February 20 [cited 2024 June 17];50(6):880-890. doi: 10.1002/eji.201948222

D. Prinz, et al., "Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2", European Journal of Immunology, vol. 50, no. 6, pp. 880-890, February 2020. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:348337. [Accessed: 17 June 2024]

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Metadata
Title (english)Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2
AuthorDaniela Prinz
AuthorKlara Klein
AuthorJulia List
AuthorVanessa M. Knab
AuthorIngeborg Menzl
AuthorNicoletta Leidenfrost
AuthorGerwin Heller
AuthorBojan Polić
AuthorEva Maria Putz
AuthorAgnieszka Witalisz‐Siepracka
AuthorVeronika Sexl
AuthorDagmar Gotthardt
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 are innate lymphocytes responsible for lysis of pathogen-infected and transformed cells. One of the major activating receptors required for target cell recognition is the NK group 2D (NKG2D) receptor. Numerous reports show the necessity of NKG2D for effective tumor immune surveillance. Further studies identified NKG2D as a key element allowing tumor immune escape. We here use a mouse model with restricted deletion of NKG2D in mature NKp46+ cells (NKG2DNK). NKG2DNK NK cells develop normally, have an unaltered IFN-γ production but kill tumor cell lines expressing NKG2D ligands (NKG2DLs) less efficiently. However, upon long-term stimulation with IL-2, NKG2Ddeficient NK cells show increased levels of the lytic molecule perforin. Thus, our findings demonstrate a dual function of NKG2D for NK cell cytotoxicity; while NKG2D is a crucial trigger for cytotoxicity of tumor cells expressing activating ligands it is also capable to limit perforin production in IL-2 activated NK cells.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleEuropean Journal of Immunology
Numberingvol. 50, no. 6, pp. 880-890
p-ISSN0014-2980
e-ISSN1521-4141
DOIhttps://doi.org/10.1002/eji.201948222
URN:NBNurn:nbn:hr:184:348337
Publication2020-02-20
Document URLhttps://onlinelibrary.wiley.com/doi/abs/10.1002/eji.201948222
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution 4.0 International (CC BY 4.0) icon
Created on2021-01-21 21:46:06