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. 2019 May 8;8(6):3012–3016. doi: 10.1002/cam4.2168

Figure 1.

Figure 1

Mechanisms of tumor progression and tumor microenvironment‐mediated immune evasion in classic Hodgkin lymphoma (cHL). Left: Programmed cell death ligand 1 (PD‐L1) normally binds PD‐1 on T cells and regulates their activity. Centre: In cHL, PD‐L1 is also expressed by Hodgkin Reed‐Sternberg (HRS) cells. In these cells, PD‐L1 binds PD‐1 on CD4 + T cells and CD8 + T cells and suppresses T‐cell effector function. Regulatory T cells (Tregs) and the PD‐1: PD‐L1 pathway are both critical to terminating immune responses. Tregs lead to inhibition of the activity of conventional T cells. Right: Infiltration of the tumor microenvironment (TME) by myeloid‐derived suppressor cells (MDSC) and CD163 + M2 macrophages inhibit immune surveillance in cHL. Inflammatory and immune cells infiltrating the TME also express ligands (eg, CD30L and CD40L) that bind receptors on HRS cell membranes. In some cases, Epstein‐Barr virus infects the tumor clone, and the viral latent membrane protein 1 (LMP1) both augments HRS cell PD‐L1 expression and helps HRS cells resist apoptosis.27 In red, therapeutic agents targeting signals that allow HRS cells to evade immune surveillance and to resist apoptosis. Asterisks indicate U.S. Food and Drug Administration approved agents