Abstract:
:Natural killer (NK) cell responsiveness in the mouse is determined in an education process guided by inhibitory Ly49 and NKG2A receptors binding to MHC class I molecules. It has been proposed that inhibitory signalling in human NK cells involves Abl-1 (c-Abl)-mediated phosphorylation of Crk, lowering NK cell function via disruption of a signalling complex including C3G and c-Cbl, suggesting that NK cell education might involve c-Abl. Mice deficient in c-Abl expression specifically in murine NK cells displayed normal inhibitory and activating receptor repertoires. Furthermore, c-Abl-deficient NK cells fluxed Ca2+ normally after triggering of ITAM receptors, killed YAC-1 tumour cells efficiently and showed normal, or even slightly elevated, capacity to produce IFN-γ after activating receptor stimulation. Consistent with these results, c-Abl deficiency in NK cells did not affect NK cell inhibition via the receptors Ly49G2, Ly49A and NKG2A. We conclude that signalling downstream of murine inhibitory receptors does not involve c-Abl and that c-Abl plays no major role in NK cell education in the mouse.
journal_name
Scand J Immunoljournal_title
Scandinavian journal of immunologyauthors
Ganesan S,Luu TT,Chambers BJ,Meinke S,Brodin P,Vivier E,Wetzel DM,Koleske AJ,Kadri N,Höglund Pdoi
10.1111/sji.12574subject
Has Abstractpub_date
2017-09-01 00:00:00pages
135-142issue
3eissn
0300-9475issn
1365-3083journal_volume
86pub_type
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