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Engagement of MHC Class I Proteins on Natural Killer Cells Inhibits their Killing Capacity
Author(s) -
PETERSSON M. G. E.,
GRÖNBERG A.,
KIESSLING R.,
FERM M. T.
Publication year - 1995
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1995.tb03622.x
Subject(s) - antibody dependent cell mediated cytotoxicity , mhc class i , major histocompatibility complex , natural killer cell , monoclonal antibody , effector , biology , microbiology and biotechnology , cytotoxicity , antibody , k562 cells , mhc restriction , chemistry , antigen , immunology , cell , biochemistry , in vitro
We have studied whether engagement of MHC class I (MHC—I) molecules on natural killer (NK) cells can influence the NK killing activity. Human NK effector cells, enriched by nylon wool passage, were incubated with monoclonal antibodies (MoAb) to MHC—I followed by cross‐linking with secondary rabbit anti mouse Ig or streptavidin. Cross linking of MHC—I molecules on NK cells resulted in a clear inhibition of the NK activity against the target cells K562, Molt‐4 and U937. The inhibitory effect was selective for MHC—I and was not seen with MoAb to MHC—II or CD56 molecules. The inhibition was not mediated via Fc receptors since F(ab) 2 fragments of the MHC—I MoAb W6/32 were as effective as the intact antibody. The best inhibition of NK activity was obtained using biotin‐labelled F(ab) 2 fragments of W6/32 and streptavidin as a cross‐linker, where up to 70 % reduction in NK cell activity was observed. Antibody dependent cellular cytotoxicity (ADCC) was also inhibited by cross‐linking MHC—I molecules on the effector cells. The results show that antibody mediated cross‐linking of MHC—I proteins on NK cells can inhibit their killing capacity. This indicates that MHC—I molecules on NK cells can be involved in the regulation of NK cytotoxicity, perhaps by transmitting inhibitory signals into the NK cell.