We investigated the presence of NK suppressor factors in HIV+ sera. We
further investigated if gp120 could be one of the substances responsi
ble for the impairment of NKC regulation found in HIV+ asymptomatic pa
tients. Our results indicate that HIV+ sera inhibit significantly norm
al NKC in a dose-dependent way, even at concentrations as low as 1%. T
he inhibitory effect of HIV+ sera decreased, but was not completely re
moved, by adsorptions of IgG or by treatment with a MoAb against human
FcIgG. Pretreatment of normal effector cells with anti-CD16 MoAb slig
htly reduced their cytotoxic capability, but did not modify the suppre
ssor effect of HIV+ sera. The preincubation of normal PBMC with recomb
inant gp120 had also a suppressor effect even at 10 ng/ml. Pretreatmen
t of HIV+ sera with anti-gp120 or anti-FcIgG MoAb reduced, but not com
pletely, their inhibitory effect. In conclusion, HIV+ serum has a dose
-dependent inhibitory effect on normal NKC. Most of this inhibition is
caused by IgG, but other substances, such as gp120, can also contribu
te to it. Since the removal of IgG and further treatments of HIV+ sera
were not able to abrogate completely the NK suppression, other serum
factors still undetermined (TNF-alpha, other cytokines), should be con
sidered.