Skip to main content
. 2019 Jun 6;10:2484. doi: 10.1038/s41467-019-10127-x

Fig. 5.

Fig. 5

PRL3-zumab recruits immune cells to tumor sites in an FcR-dependent manner. ac Orthotopic MHCC-LM3 liver tumor tissue cryo-sections from various groups of mice: I) untreated (filled black squares), II) PRL3-zumab treatment (filled red triangles), III) FcR blocker treatment (filled black triangles), and IV) PRL3-zumab plus Fc blocker combination treatment (filled black diamonds) were analyzed by immunofluorescence with antibodies against B220/CD45R (B cells; a), CD335 (NK cells; b), or F4/80 (macrophages; c) and scored for relative tumor infiltration. The mean relative infiltration was calculated using one-way analysis of variance (ANOVA) (mean ± s.e.m., n = 4 independent samples). Lower panels, representative immunofluorescence results for each antibody set. Scale bar, 200 µm. d Proposed mechanism of action of PRL3-zumab. Externalized PRL3 antigens are recognized by PRL3-zumab, which then recruits NK cells, B cells, and Ly-6C+F4/80+ macrophages for tumor killing and leakage of additional PRL3 antigens (“kill-and-leak” cycle) triggering an anti-tumor ADCC/ADCP cascade. Source data are provided as a Source Data file