Figure 8. FcγRIIB negatively regulates antibody-mediated OT-I cell priming.

(A) Diabetes incidence. RIP-mOVA or RIP-mOVA FcγRIIB^–/– mice were injected with 5 × 10⁶ OT-I cells plus either 1 mg murine polyclonal anti-OVA IgG or murine monoclonal anti-OVA IgG. For the murine monoclonal anti-OVA IgG, 6 WT and 5 FcγRIIB^–/– mice were transferred with 18 mg anti-OVA IgG2b, and 5 WT and 3 FcγRIIB^–/– mice were transferred with 42 mg anti-OVA IgG1. Fractions below bars indicate the number of diabetic mice over the total number treated. Both the murine polyclonal antibodies and mAbs showed increased diabetogenicity in mice lacking FcγRIIB. (B) OT-I cell effector differentiation. Intracellular IFN-γ staining on pancreatic lymph node OT-I cells isolated from mice 5 days after transfer of OT-I cells alone or together with 1 mg murine polyclonal anti-OVA IgG. Dot plots are gated on CD8⁺Vα2⁺Vβ5⁺ cells.