Fig. 7

Greater phagocytic capacity in CD47-deleted than in CD47-expressing macrophages. A Activation ( →) and inhibition (_┴) of myelin debris phagocytosis—a schematic view. Wild type myelin (WT myelin) from wild type mice, either or not opsonized by complement protein C3bi (± C3bi), binds and activates CR3 that mediates much of the phagocytosis of myelin debris in context of traumatic injury [4,5,6]. CD47 on WT myelin (a) and serum (b) trigger each SIRPα-dependent phagocytosis inhibition in wild type macrophages (WT phagocytes). Tested hypothesis (c): CD47 on phagocytes triggers phagocytosis inhibition. A potential ligand that could activate CD47 is thrombospondin-1 (TSP1; see Discussion). B and C Phagocytosis in serum-free medium of myelin debris from (B) CD47−/− mice (CD47−/− myelin) and from (C) wild type mice (WT myelin) by WT and CD47−/− macrophages from WT and CD47−/− mice. In each experimental paradigm, phagocytosis levels in WT macrophages were normalized to 100% and phagocytosis levels in CD47−/− macrophages presented as percentage of phagocytosis in WT macrophages. Box and whisker plots of (B) 24 replicates in 7 experiments, (C) 18 replicated in 6 experiments. Significance of difference between WT and CD47−/− macrophages is ***p < 0.001, by unpaired t test. In CD47−/− macrophages, the 2.3-fold phagocytosis augmentation of CD47−/− myelin and the 1.7-fold phagocytosis augmentation of WT myelin differed one from the other significantly (p < 0.01, by unpaired t test; not marked in figure)