IVIg did not inhibit T-cell responses by direct interaction with T cells. (A) IFN-γ–stimulated P388D1 cells were incubated in the presence of IVIg (10 mg/mL) or the corresponding volume of RPMI 1640 medium (control), for 24 hours. IVIg (or RPMI) was then removed and DO-11.10 hybridoma cells were added with OVA-IC for an additional 24 hours. DO-11.10 cell activation was measured by IL-2 secretion. (B) IFN-γ–stimulated P388D1 cells were pulsed with OVA-ICs for 24 hours and fixed with paraformaldehyde. DO-11.10 cells were then added in the presence or not of IVIg (10 mg/mL), and IL-2 secretion was measured 24 hours later. (C) OVA-specific CD4⁺ T cells isolated from spleens of DO11.10 mice were cultured with OVA-IC—pulsed, P388D1-fixed cells in the presence or not of IVIG (10 mg/mL). IL-2 secretion was measured 24 hours later. (D-E) CFSE-stained spleen cells from naive BALB/c mice were incubated with or without Dynabeads Mouse CD3/CD28 T-cell expander in the presence or absence of IVIg (10 mg/mL): (D) polyclonal T-cell activation was evaluated by measuring IL-2 secretion 24 hours later, and (E) T-cell proliferation was evaluated by analysis of CFSE dilution by flow cytometry after 72 hours of culture. All results are representative of 2 independent experiments. *P < .001.