Fig. 4.
Fig. 4. Defective APC function in anti-CD3ɛ–treated mice. Spleen cells from control antibody-treated or anti-CD3ɛ–treated BALB/c mice (50 μg IV) were irradiated and used as accessory cells to stimulate (A and B) G10-nonadherent responding cells from CBA mice (3 × 105/well) or (C) ovalbumin-specific T-cell hybridoma mice (3 × 105/well) in the presence of 1 μg/mL of ovalbumin peptide. Proliferation (A) and IL-2 production (B and C) were assayed as described in Materials and Methods. Results are expressed as counts per minute (cpm) of [3H] TdR incorporation by responder cells (A) or IL-2–dependent cell line CTL.L (B and C). These results are representative of 3 independent experiments.

Defective APC function in anti-CD3ɛ–treated mice. Spleen cells from control antibody-treated or anti-CD3ɛ–treated BALB/c mice (50 μg IV) were irradiated and used as accessory cells to stimulate (A and B) G10-nonadherent responding cells from CBA mice (3 × 105/well) or (C) ovalbumin-specific T-cell hybridoma mice (3 × 105/well) in the presence of 1 μg/mL of ovalbumin peptide. Proliferation (A) and IL-2 production (B and C) were assayed as described in Materials and Methods. Results are expressed as counts per minute (cpm) of [3H] TdR incorporation by responder cells (A) or IL-2–dependent cell line CTL.L (B and C). These results are representative of 3 independent experiments.

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