Suppression of cytokine-dependent XXXX T-cell proliferation by intravenous immunoglobulin.

@entity1 @entity4621 @entity1360 @entity1199 @entity3646 @entity116
@entity1 intravenous immunoglobulin (hIVIG) modifies the course of numerous immune-mediated diseases, but its specific mode of action remains unknown. In order to delineate possible immunoregulatory mechanisms, we studied the effects of hIVIG on the in vitro proliferation of @entity1 T cells. Cells from normal donors were stimulated with anti-CD3 antibody, @entity116 toxoid antigen or the combination of a @entity4621 / @entity1360 (P/I) and incubated with increasing concentrations of hIVIG (1 mg/ml to 10 mg/ml) for three to seven days. Addition of hIVIG inhibited anti-CD3 and @entity116 but not P/I-induced proliferation in a dose-dependent manner. Addition of exogenous @entity1199 to the cultures overcame the inhibitory effect of hIVIG; addition of @entity3646 was ineffective. To further define the effect of hIVIG on specific cell populations, competent, purified T cells were stimulated with anti-CD3 or @entity4621 for three days in the presence of hIVIG. Addition of hIVIG blocked anti-CD3 and @entity4621 -induced stimulation of competent T cells. In cultures of competent T cells, either @entity1199 or @entity3646 was successful in reversing the hIVIG-induced inhibition. In these cultures, hIVIG also significantly prevented the synthesis/secretion of both @entity1199 and @entity3646 in PDB-stimulated competent T cells. Taken together, these data suggest that one mechanism of action of hIVIG may be through its interference with cytokine-dependent T-cell proliferation.
