CHEMOSPECIFICITY AND CROSS-REACTIVITY OF TARGET-CELL RECOGNITION BY HUMAN CD56(+) NK AND LAK CELLS

Inhibition of specific cytotoxicity of highly purified (> 95%) human C D56(+) NK and LAK cells against K562 tumour cells was studied with var ious sugar acetates. Maximum inhibitory specificity was obtained with 60%-deacetylated penta-acetates of mannose, galactose, glucose, or 80% -deacetylated penta-O-acetate of N-acetyl neuraminic acid. The inhibit ion was strictly dosedependent and 100% inhibition was achieved in the concentration range of 500-1000 nmoles/ml with all four sugar acetate samples. Enhancement of specific cytotoxicity in the presence of rham nogalacturonan (RG; 500 ng/ml), acting as a bridging molecule, was als o inhibited in a dose-dependent manner with the same inhibitory specif icity and within the same concentration range indicating involvement o f the same number of sugar acetate-specific receptors. Moreover, forma tion of lytic CD56(+) effector cell/tumour cell (E/T) conjugates was e qually well inhibited whereas formation of total E/T conjugates was on ly partially inhibited (NK: 44-73%; LAK: 46-50%). E/T conjugate format ion in the presence of RG was enhanced. Inhibition of the enhancement of formation of lytic E/T conjugates in the presence of RG was again c ompletely accomplished with the same inhibitory specificity and within the same concentration ranges as recorded for E/T conjugate formation in the absence of RG. However, inhibition of total E/T conjugate form ation was again only partially achieved at the given concentrations. T he data support the assumption of an NK cell receptor with specificity for acetylated carbohydrate moieties on target cells or on bridging m olelcules such as RG.