Chemospecificity and Cross-Reactivity of Target Cell Recognition by Human CD56+ NK and LAK Cells

Inhibition of specific cytotoxicity of highly purified (> 95%) human CD56⁺ NK and LAK cells against K562 tumour cells was studied with various sugar acetates. Maximum inhibitory specificity was obtained with 60%-deacetylated penta-acetates of mannose, galactose, glucose, or 80%-deacetylated penta-O-acetate of N-acetyt neuraminic acid. The inhibition 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 rhamnogalacturonan (RG; 500 ng/ml), acting as a bridging molecule, was also inhibited in a dose-dependent manner with the same inhibitory specificity and within the same concentration range indicating involvement of the same number of sugar acetate-specific receptors. Moreover, formation of lytic CD56⁺ effector cell/tumour cell (E/T) conjugates was equally well inhibited whereas formation of total E/T conjugates was only partially inhibited (NK: 44–73%; LAK: 46–50%). E/T conjugate formation 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 completely 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 formation was again only partially achieved at the given concentrations. The data support the assumption of an NK cell receptor with specificity for acetylated carbohydrate moieties on target cells or on bridging molelcules such as RG.