Figure 4
Figure 4. OA inhibits cytokine-enhanced FcγRI IC binding on primary monocytes and Ba/F3- FcγRI cells. (A) Ba/F3-FcγRI cells were treated with DMSO, LY294002 (LY), U-0126 (U0) or OA and stimulated with IL-3. IC Binding was tested using mIgG2a-opsonized RBCs. Data represent means of at least 4 replicates. Similar results were obtained in 3 independent experiments. **P < .01; ***P < .01; NS: not significant. (B) IFNγ stimulated monocyte binding to mIgG2a-opsonized RBCs after OA treatment. ***P < .001, comparing 1μM OA treatment with DMSO fitted curve; NS: not significant, comparing 0.1μM OA treatment with DMSO treated fitted curve. (C) Effect of FcγRI blocking mAb 10.1 binding of mIgG2a-opsonized RBCs to FcγRI. Similar results were seen in 3 independent experiments.

OA inhibits cytokine-enhanced FcγRI IC binding on primary monocytes and Ba/F3- FcγRI cells. (A) Ba/F3-FcγRI cells were treated with DMSO, LY294002 (LY), U-0126 (U0) or OA and stimulated with IL-3. IC Binding was tested using mIgG2a-opsonized RBCs. Data represent means of at least 4 replicates. Similar results were obtained in 3 independent experiments. **P < .01; ***P < .01; NS: not significant. (B) IFNγ stimulated monocyte binding to mIgG2a-opsonized RBCs after OA treatment. ***P < .001, comparing 1μM OA treatment with DMSO fitted curve; NS: not significant, comparing 0.1μM OA treatment with DMSO treated fitted curve. (C) Effect of FcγRI blocking mAb 10.1 binding of mIgG2a-opsonized RBCs to FcγRI. Similar results were seen in 3 independent experiments.

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