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. 2021 Feb 16;9(2):e001230. doi: 10.1136/jitc-2020-001230

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© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution 4.0 Unported (CC BY 4.0) license, which permits others to copy, redistribute, remix, transform and build upon this work for any purpose, provided the original work is properly cited, a link to the licence is given, and indication of whether changes were made. See https://creativecommons.org/licenses/by/4.0/.

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Non-canonical programmed cell death 1 (PD-1) signaling in tumorous B cells. Hepatocellular carcinoma (HCC) factors induce PD-1^high B cells through TLR4-driven Bcl-6 upregulation. By engagement with PD-L1, non-canonical PD-1 signaling in B cells inhibits antitumor immunity by enhancing IL-10 production. PD-1 blockade decreases interleukin (IL)-10 production and promotes proliferation and differentiation into a memory phenotype of B cells, which may influence efficacy of PD-1 blockade therapy.