Paclitaxel resensitized the response of aCD47 in NHL-bearing mice. (A) A schematic showing the treatment strategy of the subcutaneous NHL models. Growth of tumors derived from Raji cells in RAG2^−/−γc^−/− mice (B) and A20 cells in BALB/c mice (C). Mice subcutaneously engrafted with Raji cells or A20 cells were treated with control vehicle, aCD47, paclitaxel, or a combination of aCD47 and paclitaxel. Tumor growth was measured by bioluminescence imaging; *P < .05; ***P < .001 (log-linear regression analysis). (D) A schematic showing the treatment strategy (top); a single dose of nab-paclitaxel (50 mg/kg) largely enhanced the efficacy of aCD47 in mice bearing systemic NHL disease (bottom). *P < .05; ***P < .001 (1-way ANOVA test). (E) A single nontoxic dose of nab-paclitaxel (25 mg/kg) was sufficient to enhance the response to aCD47 in reducing tumor burden. *P < .05 (1-way ANOVA test). (F) Depletion of BM macrophages with clodronate liposome abolished the therapeutic effect of nab-paclitaxel and aCD47 combination. **P < .01, ***P < .001 (1-way ANOVA test). ns, not significant.