prikaz prve stranice dokumenta Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice
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Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice
Immunity, 31 (2009), 2; 270-282. https://doi.org/10.1016/j.immuni.2009.06.017
Zafirova, Biljana; Mandarić, Sanja; Antulov, Ronald; Krmpotić, Astrid; Jonsson, Helena; Yokoyama, Wayne M.; Jonjić, Stipan; Polić, Bojan

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Zafirova, B., Mandarić, S., Antulov, R., Krmpotić, A., Jonsson, H., Yokoyama, W. M. ... Polić, B. (2009). Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice. Immunity, 31. (2), 270-282. doi: 10.1016/j.immuni.2009.06.017

Zafirova, Biljana, et al. "Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice." Immunity, vol. 31, br. 2, 2009, str. 270-282. https://doi.org/10.1016/j.immuni.2009.06.017

Zafirova, Biljana, Sanja Mandarić, Ronald Antulov, Astrid Krmpotić, Helena Jonsson, Wayne M. Yokoyama, Stipan Jonjić i Bojan Polić. "Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice." Immunity 31, br. 2 (2009): 270-282. https://doi.org/10.1016/j.immuni.2009.06.017

Zafirova, B., et al. (2009) 'Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice', Immunity, 31(2), str. 270-282. doi: 10.1016/j.immuni.2009.06.017

Zafirova B, Mandarić S, Antulov R, Krmpotić A, Jonsson H, Yokoyama WM, i sur.. Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice. Immunity [Internet]. 08.2009. [pristupljeno 28.11.2024.];31(2):270-282. doi: 10.1016/j.immuni.2009.06.017

B. Zafirova, et al., "Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice", Immunity, vol. 31, br. 2, str. 270-282, Kolovoz 2009. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:184:142440. [Citirano: 28.11.2024.]

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Naslov (engleski)Altered NK Cell Development and Enhanced NK Cell-Mediated Resistance to Mouse Cytomegalovirus in NKG2D-Deficient Mice
AutorBiljana Zafirova
AutorSanja Mandarić
AutorRonald Antulov
AutorAstrid Krmpotić
AutorHelena Jonsson
AutorWayne M. Yokoyama
AutorStipan Jonjić
AutorBojan Polić
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)
NKG2D is a potent activating receptor on natural killer (NK) cells and acts as a molecular sensor for stressed cells expressing NKG2D ligands such as infected or tumor-transformed cells. Although NKG2D is expressed on NK cell precursors, its role in NK cell development is not known. We have generated NKG2D-deficient mice by targeting the Klrk1 locus. Here we provide evidence for an important regulatory role of NKG2D in the development of NK cells. The absence of NKG2D caused faster division of NK cells, perturbation in size of some NK cell subpopulations, and their augmented sensitivity to apoptosis. As expected, Klrk1(-/-) NK cells are less responsive to tumor targets expressing NKG2D ligands. Klrk1(-/-) mice, however, showed an enhanced NK cell-mediated resistance to mouse cytomegalovirus infection as a consequence of NK cell dysregulation. Altogether, these findings provide evidence for regulatory function of NKG2D in NK cell physiology.
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran - međunarodna recenzija
Verzija publikacijeObjavljena verzija rada (izdavačev PDF)
Naslov časopisaImmunity
Brojčani podacivol. 31, br. 2, str. 270-282
p-ISSN1074-7613
DOIhttps://doi.org/10.1016/j.immuni.2009.06.017
URN:NBNurn:nbn:hr:184:142440
Datum objave publikacije2009-08
URL dokumentahttp://linkinghub.elsevier.com/retrieve/pii/S107476130900315X
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
Uvjeti korištenjaIkona licence Imenovanje-Nekomercijalno-Bez prerada 4.0 međunarodna (CC BY-NC-ND 4.0)
Datum i vrijeme pohrane2018-11-08 20:03:51