The function of human NK cells is enhanced by beta-glucan, a ligand of CR3 (CD11b/CD18).
Cells responsible for the natural killer (NK) effect in the human blood can be collected in the low-density lymphocyte subset and the majority of them express CR3. In addition to the iC3b binding site the CR3 molecules possess an epitope which binds beta-glucan. Ligands of this site can deliver activation signals to CR3-carrying monocytes and neutrophils. We found that the function of NK cells was also potentiated by preincubation with beta-glucan. The treatment increased the proportion of target-binding lymphocytes and of the damaged target cells in the conjugates. The monoclonal antibody OKM-1, directed to the beta-glucan-binding site of CR3, abrogated this effect. Another CR3-reactive monoclonal antibody, M522, known to activate monocytes and neutrophils, enhanced the NK function.
Di Renzo
L
L
Department of Tumor Biology, Karolinska Institutet, Stockholm, Sweden.
Yefenof
E
E
Klein
E
E
D000911:Antibodies, Monoclonal / Q000276:immunology; D003602:Cytotoxicity, Immunologic / Q000187:drug effects; D005936:Glucans / Q000494:pharmacology*; D006801:Humans; D007694:Killer Cells, Natural / Q000187:drug effects* / Q000276:immunology; D016177:Macrophage-1 Antigen / Q000502:physiology*
D000911:Antibodies, Monoclonal; D005936:Glucans; D016177:Macrophage-1 Antigen