Fig. 5.
Fig. 5. Role of CRs and complement in uptake of apoptotic cells by splenic DCs. / (A) Internalization of apoptotic BALB/c splenocytes by purified splenic B10 DCs in the presence of mAb specific for CR or controls. Apoptotic cells were preincubated with normal mouse B10 serum before analysis, and phagocytosis assays were conducted in the presence of vol/vol 10% heat-inactivated mouse B10 serum. Uptake of apoptotic cells (percent) relative to control represents the percentage of DCs with apoptotic cells in each experimental condition compared with the control group performed in the absence of mAbs and considered as 100% of phagocytosis (dotted line). Data represent the means ± SDs of 3 experiments; *P ≤ .01; **P ≤  .001. (B-C) B10 mice made hypocomplementemic with CVF were injected intravenously with PKH67-BALB/c apoptotic splenocytes. After 12 hours, the animals were killed and splenic DC-enriched suspensions were stained with phycoerythrin–anti-CD11c mAb. As controls, non-CVF–treated animals injected with the same dose of apoptotic cells were included. Data in panel B are from one animal representative of each group (n = 8). The percentages of splenic DCs with apoptotic cells in individual animals of each group and their means ± SDs are displayed in panel C.

Role of CRs and complement in uptake of apoptotic cells by splenic DCs.

(A) Internalization of apoptotic BALB/c splenocytes by purified splenic B10 DCs in the presence of mAb specific for CR or controls. Apoptotic cells were preincubated with normal mouse B10 serum before analysis, and phagocytosis assays were conducted in the presence of vol/vol 10% heat-inactivated mouse B10 serum. Uptake of apoptotic cells (percent) relative to control represents the percentage of DCs with apoptotic cells in each experimental condition compared with the control group performed in the absence of mAbs and considered as 100% of phagocytosis (dotted line). Data represent the means ± SDs of 3 experiments; *P ≤ .01; **P ≤  .001. (B-C) B10 mice made hypocomplementemic with CVF were injected intravenously with PKH67-BALB/c apoptotic splenocytes. After 12 hours, the animals were killed and splenic DC-enriched suspensions were stained with phycoerythrin–anti-CD11c mAb. As controls, non-CVF–treated animals injected with the same dose of apoptotic cells were included. Data in panel B are from one animal representative of each group (n = 8). The percentages of splenic DCs with apoptotic cells in individual animals of each group and their means ± SDs are displayed in panel C.

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