INHIBITION OF ANTI-GD3-GANGLIOSIDE ANTIBODY-INDUCED PROLIFERATION OF HUMAN CD8(-CELLS BY CD16(+) NATURAL-KILLER-CELLS() T)

The ganglioside GD3 has been described as a membrane component of huma n T cells which is involved in T cell growth. In the present study the activating function of GD3 for human CD4(+) and CD8(+) T cells was an alyzed by five different monoclonal antibodies (mAb) directed against the GD3 molecule. Three mAb U5, Z21 and R24 induced strong proliferati on of peripheral blood mononuclear cells and purified CD8(+) and CD4() T cells of normal donors containing less than 5% CD16(+) natural kil ler (NK) cells. In contrast to CD4(+) T cells, CD8(+) T cells prolifer ated only weakly in the presence of 15% CD16(+) NK cells. The prolifer ative response of purified CD4(+) and CD8(+) T cells (<5% NK cells) co rrelated with the antibody-dependent induction of integral and soluble interleukin-2 (IL-2) receptors and was reduced to 20% by an anti-IL-2 receptor antibody. Our results show, that the GD3 molecule represents an activation molecule for both CD4+ and CD8(+) T cells and that CD16 (+) NK cells selectively inhibit anti-GD3 antibody-induced proliferati on of CD8(+) T cells.