Fig. 7.
Fig. 7. Effect of an anti–MD-1 mAb on LPS-induced B-cell proliferation. / Purified spleen B cells were stimulated for 3 days with anti-CD40 (10 μg/mL); anti-IgM (10 μg/mL); anti-RP105 (2 μg/mL); lipid A (0.01, 0.1, and 1.0 μg/mL); LPS from S minnesota Re595 or E coli 055: B5 (0.01, 0.1, and 1.0 μg/mL). Anti–MD-1 mAb MD88 (10 μg/mL) was included in the groups shown with closed bars. [3H]-TdR uptake was counted as described in “Materials and methods.” Results were represented by mean cpm values from triplicate wells with standard errors. When compared with B cells cultured without antibody, B cells cultured in the presence of the anti–MD-1 mAb showed significant hyporesponsiveness to LPS as revealed by the following P values: lipid A 0.01 μg/mL,P < .003; Re595 1.0 μg/mL, P < .012; Re595 0.1 μg/mL, P < .010; Re595 0.01 μg/mL,P < .003; 055:B5 0.01 μg/mL, P < .005; 055:B5 0.1 μg/mL, P < .001.; 055:B5 1.0 μg/mL,P < .001.

Effect of an anti–MD-1 mAb on LPS-induced B-cell proliferation.

Purified spleen B cells were stimulated for 3 days with anti-CD40 (10 μg/mL); anti-IgM (10 μg/mL); anti-RP105 (2 μg/mL); lipid A (0.01, 0.1, and 1.0 μg/mL); LPS from S minnesota Re595 or E coli 055: B5 (0.01, 0.1, and 1.0 μg/mL). Anti–MD-1 mAb MD88 (10 μg/mL) was included in the groups shown with closed bars. [3H]-TdR uptake was counted as described in “Materials and methods.” Results were represented by mean cpm values from triplicate wells with standard errors. When compared with B cells cultured without antibody, B cells cultured in the presence of the anti–MD-1 mAb showed significant hyporesponsiveness to LPS as revealed by the following P values: lipid A 0.01 μg/mL,P < .003; Re595 1.0 μg/mL, P < .012; Re595 0.1 μg/mL, P < .010; Re595 0.01 μg/mL,P < .003; 055:B5 0.01 μg/mL, P < .005; 055:B5 0.1 μg/mL, P < .001.; 055:B5 1.0 μg/mL,P < .001.

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