PD-1 Shapes B Cells as Evildoers in the Tumor Microenvironment

Abstract

Protumorigenic PD-1(hi) B cells, induced in hepatocellular carcinoma, suppress tumor-specific T-cell response via IL10-dependent pathways upon PD-1/PD-L1 interaction. Anti-PD-1 or anti-PD-L1 antibodies may function not only through blocking the PD-1 coinhibitory pathway in T cells but also via abolishing the suppressive function of regulatory B cells. Cancer Discov; 6(5); 477-8. ©2016 AACRSee related article by Xiao et al., p. 546.

Figure 1

The role of PD-1/PD-L1 interaction in suppressing tumor-specific T cell and the potential mechanism of how anti-PD-1/anti-PD-L1 works in tumor treatment. A. By interacting directly with PD-L1⁺ monocytes or macrophages, the PD-1^high B cells induce T cell dysfunction via IL-10-dependent pathways and PD-L1⁺ monocytes or macrophages can also directly induce the T cell dysfunction by PD-L1/PD-1 interaction. B. Anti-PD-1 or anti-PD-L1 antibody can block the PD-1/PD-L1 interactions of T cell or PD-1^high B cells with monocytes or macrophage, which rescues the function of effector T cells.