Naslov
Comparable NK-cell phenotype of Klrk1D/D to the Klrk1-/- mice

Autori
Zafirova, Biljana ; Gulin, Maja ; Jonjić, Stipan ; Polić, Bojan

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
12th Meeting of the Society for Natural Immunity / Jonjić, Stipan ; Waltz, Carsten ; Krmpotić, Astrid ; Polić, Bojan - Rijeka, 2010

Skup
12th Meeting of the Society for Natural Immunity

Mjesto i datum
Dubrovnik, Hrvatska; Cavtat, Hrvatska, 11.09.2010. - 15.09.2010

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
NK cells; NKG2D-deficiency; Klrk1flox/flox mice mutant; Klrk1D/D mice mutant

Sažetak
NKG2D is a potent acitvating receptor implicated in the efficient NK cell-mediated control of transformed or virally infected cells. It is expressed already on NK cell precursorsand virtually all NK cells increase NKG2D expression during the immature phase of their development. In our model of NKG2D- deficiency (B.Zafirova et al. (2009), Immunity) we have shown a dual role of NKG2D in the physiology of NK cells: one rather regulatory, implicated in their development, homeostasis and survival, and other, important for exerting their effector functions. We have observed following consequences of NKG2D deficiency on the NK cell development and homeostasis: a) faster division of NK cells, b) perturbation in size of NK cell subpopulations and, c) their augmented sensitivity to apoptosis. NKG2D- mediated cytotoxicity and cytokine production of the NKG2D-deficient NK cells was abolished in vitro. Unexpectedly, Klrk1-/- mice have shown enhanced NK cell-mediated resistance to MCMV infection. In order to check whether the observed phenotype is a consequence of the introduced EGFP sequence in the third exon of Klrk1-/- locus, we analyzed Klrk1 mouse mutant obtained from a different targeting experiment. We have generated Klrk1 conditional mouse mutant by introducing loxP sites in the first and third intron. The Klrk1flox/flox mice were bred with the Cre deleter mice to obtain Klrk1D/D mice lacking the second and third exons containing ATG sites. Analysis of these mice showed similar pattern of perturbation in NK cell subpopulations during the development as well as enhanced NK cell-mediated control of MCMV. Thus, these data strongly support the relevance of Klrk1 mutation itself for the observed phenotype in Klrk1-/- mice and exclude potential influence of EGFP as a foreign genetic element.

Izvorni jezik
Engleski

Znanstvena područja
Biologija

POVEZANOST RADA