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Absolute requirement of CD11/CD18 adhesion molecules, FcRII and the
phosphatidylinositol-linked FcRIII for monoclonal antibody-mediated
neutrophil antihuman tumor cytotoxicity
BH Kushner and NK Cheung
Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York
NY 10021.
We have previously shown that 3F8, a murine IgG3, monoclonal antibody
(MoAb) specific for the ganglioside GD2, mediates tumor cell kill in vitro
and in vivo. We now describe receptor requirements of polymorphonuclear
leukocytes (PMN) in 3F8-mediated cytotoxicity (ADCC) of human GD2 (+)
melanoma and neuroblastoma cell lines. PMN from a child with leukocyte
adhesion deficiency (LAD) were devoid of CD11/CD18 adhesion molecules and
mounted no detectable ADCC. MoAb to CD11b, CD11c, and CD18 each efficiently
blocked ADCC by normal PMN. In contrast, a panel of different MoAbs to
CD11a had no significant inhibitory effect on ADCC, a finding consistent
with the low-to-absent expression of the CD11a ligand, intercellular
adhesion molecule-1, on the target cells. Granulocyte-macrophage
colony-stimulating factor (GM- CSF) significantly increased the expression
of CD11b, CD11c, and CD18 on normal PMN, decreased the expression of Fc
receptors (FcR), and enhanced ADCC by normal but not by LAD PMN. MoAbs to
FcRII and FcRIII each efficiently blocked ADCC; anti-FcRI MoAb had no
effect. Flow cytometry using anti-FcRII MoAb versus anti-FcRIII MoAb did
not show cross competition, suggesting that inhibition of ADCC was not a
steric effect resulting from FcRII proximity to FcRIII. PMN deficient in
FcRIII (obtained from patients with paroxysmal nocturnal hemoglobinuria)
and PMN depleted of FcRIII by treatment with elastase or
phosphatidylinositol (PI)-specific phospholipase C produced low ADCC,
supporting a role for the PI-liked FcRIII. Thus, optimal ADCC using human
PMN, human solid tumor cells, and a clinically active MoAb (conditions that
contrast with the heterologous antibodies and nonhuman or nonneoplastic
targets used in most models of PMN ADCC) required CD11b, CD11c, FcRII, and
the PI-linked FcRIII. Furthermore, in this clinically relevant system,
GM-CSF enhancement of antitumor PMN ADCC correlated with increased
expression of CD11/CD18 molecules.
Volume 79,
Issue 6,
pp. 1484-1490,
03/15/1992
Copyright © 1992 by The American Society of Hematology
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