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. 2019 Aug 5;17:89. doi: 10.1186/s12964-019-0391-x

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — Graphical representation of signaling pathways leading to PD-L1 over-expression in tumor B-cells from LMP1/CD40 mice. CD19, BCR (B-cell receptor), Igαβ, LMP1/CD40, and IL-10R (IL-10 receptor) are located at the surface membrane. CD19 plus BCR/Igαβ complex, and CD40 lead to BTK (Burton’s tyrosine kinase) activation which in turn activate ERK and NF-κB that up-regulate PD-L1 expression. Indirectly PD-L1 is also increase by IL-10 by an autocrine loop. PHA-408, inhibitor of NF-κB. Ruxolitinib, inhibitor of JAK1/JAK2. Ibrutinib, inhibitor of BTK