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Altered NK cell Development and Enhanced NK Cell-Mediated Resistance to MCMV in NKG2D-Deficient Mice (CROSBI ID 153093)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Zafirova, Biljana ; Mandarić, Sanja ; Antulov, Ronald ; Krmpotić, Astrid ; Jonsson, Helena ; Yokoyama, Wayne M ; Jonjić, Stipan ; Polić, Bojan Altered NK cell Development and Enhanced NK Cell-Mediated Resistance to MCMV in NKG2D-Deficient Mice // Immunity, 31 (2009), 2; 270-282

Podaci o odgovornosti

Zafirova, Biljana ; Mandarić, Sanja ; Antulov, Ronald ; Krmpotić, Astrid ; Jonsson, Helena ; Yokoyama, Wayne M ; Jonjić, Stipan ; Polić, Bojan

engleski

Altered NK cell Development and Enhanced NK Cell-Mediated Resistance to MCMV in NKG2D-Deficient Mice

NKG2D is a potent activating receptor on NK cells which acts as a molecular sensor for stress exposed 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 still not known. We have generated NKG2D-deficient mice by targeting the Klrk-1 locus. Here we provide evidence for an important regulatory role of NKG2D in the development of NK cells. The absence of NKG2D causes considerably faster division of NK cells, perturbation in size of some NK cell subpopulations and their augmented sensitivity to apoptosis. As expected, NKG2D-/- NK cells are less responsive to tumor targets expressing NKG2D ligands. NKG2D-/- mice, however, show an enhanced NK cell-mediated resistance to MCMV infection as a consequence of NK cell dysregulation. Altogether, these findings provide evidence for yet unknown regulatory function of NKG2D in NK cell physiology.

NKG2D-deficient mice; NKG2D; NK cells; NK cell development; proliferation; apoptosis; MCMV

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Podaci o izdanju

31 (2)

2009.

270-282

objavljeno

1074-7613

Povezanost rada

Temeljne medicinske znanosti, Biotehnologija

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