Fig. 5.
Fig. 5. Inhibition of Id-induced IFN-γ (P1, P2, P4, P5) or IL-2 (P3) cytokine–secreting cells by MHC antibodies (ELISPOT) (mean + SEM). PBMC were stimulated in vitro by F(ab′)2 fragments of the autologous monoclonal IgG (10 pg/mL) in the presence or absence of mouse MoAbs against human MHC class II (▪), MHC class I molecules (▨), or control mouse IgG2b (□) (1 μg/mL). The absolute number of cells/105 PBMC after stimulation with the autologous monoclonal IgG (in the absence of blocking antibodies) for patient nos. 1 through 5 were 18, 30, 22, 16, and 19 cells, respectively. The corresponding numbers obtained with isotypic control IgG were 3, 1, 4, 2, and 3 cells, respectively. Results are expressed as percent inhibition compared with cells incubated without the blocking MoAbs.

Inhibition of Id-induced IFN-γ (P1, P2, P4, P5) or IL-2 (P3) cytokine–secreting cells by MHC antibodies (ELISPOT) (mean + SEM). PBMC were stimulated in vitro by F(ab′)2 fragments of the autologous monoclonal IgG (10 pg/mL) in the presence or absence of mouse MoAbs against human MHC class II (▪), MHC class I molecules (▨), or control mouse IgG2b (□) (1 μg/mL). The absolute number of cells/105 PBMC after stimulation with the autologous monoclonal IgG (in the absence of blocking antibodies) for patient nos. 1 through 5 were 18, 30, 22, 16, and 19 cells, respectively. The corresponding numbers obtained with isotypic control IgG were 3, 1, 4, 2, and 3 cells, respectively. Results are expressed as percent inhibition compared with cells incubated without the blocking MoAbs.

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