We aimed to investigate the natural killer (NK) cell activity in
hGH-deficient adults and to analyze the effect of insulin-like growth
factor (IGF)-I in uivo and in vitro on NK cell activity. NK cell activity
was measured in a 4-h nonisotopic assay with europium-labeled and
cryopreserved K-562 cells. NK-cell numbers were measured after
incubation with murine monoclonal CD3 and CD16 antibodies by flow
cytometry analysis. In a cross-sectional study, the basal and interferon-
p (IFN-P) stimulated (1000 IU/ml) NK cell activity of 15 hGHdeficient
patients and 15 age- and sex-matched controls was measured.
The percentages and absolute numbers of CD3./16+ NK-cells
were not significantly different in the patient vs. control group. The
basal and IFN-P stimulated NK cell activity however was significantly
decreased in the patient vs. control group at all effecter/target
(E/T) cell ratios from 12.5-100 (e.g. 17 ? 3 vs. 28 ? 3% lysis without
IFN-P, P < 0.05, and 42 t 4 vs. 57 2 4% lysis with IFN-0, P < 0.05;
both at E/T 50). IGF-I levels of patients and controls showed a significant
positive correlation with NK cell activity (r = 0.37; P < 0.05).
In an IGF-I in vitro study (IGF-I in vitro 250-1250 kg/L), the basal and
IFN-P stimulated NK cell activity of 13 hGH-deficient patients and of
18 normal subjects was significantly enhanced by IGF-I in vitro (e.g.
GH-deficient patients: 9 ? 2 us. 10 2 2% lysis without IFN-P, P < 0.05
and 25 + 4 vs. 30 + 4% lysis with IFN-/3, P < 0.005; and normal
subjects: 15 + 3 vs. 23 ? 3% lysis without IFN-/3, P < 0.001 and 35 2
4 us. 44 + 5% lysis with IFN-P, P < 0.001; both at IGF-I 500 pg/L).
In summary, in our cross-sectional study, adult GH-deficient patients
showed a significantly lower basal and IFN-P stimulated NK cell
activity than matched controls, despite equal NK cell numbers. IGF-I
levels of patients and controls showed a weak positive correlation with
NK cell activity. In an in vitro study, IGF-I significantly enhanced
basal and IFN-P stimulated NK cell activity of hGH-deficient patients
and also of normal subjects. The decreased NK cell activity in GHdeficient
patients may be caused at least in part by low serum IGF-I
levels. IGF-I appears to be an independent coregulatory modulator of
NK cell activity. (Endocrinology 137: 5332-5336, 1996
