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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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, br. 6, 2020, str. 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, br. 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), str. 880-890. doi: 10.1002/eji.201948222

Prinz D, Klein K, List J, Knab VM, Menzl I, Leidenfrost N, i 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]. 20.02.2020. [pristupljeno 26.12.2024.];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, br. 6, str. 880-890, Veljača 2020. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:184:348337. [Citirano: 26.12.2024.]

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Naslov (engleski)Loss of NKG2D in murine NK cells leads to increased perforin production upon long‐term stimulation with IL‐2
AutorDaniela Prinz
AutorKlara Klein
AutorJulia List
AutorVanessa M. Knab
AutorIngeborg Menzl
AutorNicoletta Leidenfrost
AutorGerwin Heller
AutorBojan Polić
AutorEva Maria Putz
AutorAgnieszka Witalisz‐Siepracka
AutorVeronika Sexl
AutorDagmar Gotthardt
Autorova ustanovaSveučilište u Rijeci
Medicinski fakultet
(Katedra za histologiju i embriologiju)
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Sažetak (engleski)
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.
Ključne riječi (engleski)
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran - međunarodna recenzija
Verzija publikacijeObjavljena verzija rada (izdavačev PDF)
Naslov časopisaEuropean Journal of Immunology
Brojčani podacivol. 50, br. 6, str. 880-890
p-ISSN0014-2980
e-ISSN1521-4141
DOIhttps://doi.org/10.1002/eji.201948222
URN:NBNurn:nbn:hr:184:348337
Datum objave publikacije2020-02-20
URL dokumentahttps://onlinelibrary.wiley.com/doi/abs/10.1002/eji.201948222
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
Uvjeti korištenjaIkona licence Imenovanje 4.0 međunarodna (CC BY 4.0)
Datum i vrijeme pohrane2021-01-21 21:46:06