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. 2021 Jul 21;36(1):138–154. doi: 10.1038/s41375-021-01301-6

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — BMMC from MM patients were treated with clinical grade checkpoint inhibitor or immune agonist in the presence of low level of IL-2 (20 units/ml) and examined for checkpoint expression and immune function. A Treatment of BMMC from MM patients (N = 10) with anti-PD1, anti-LAG3, anti-OX40, or anti-GITR increased expansion of T cells expressing another immune checkpoint. B Treatment of BMMC of MM patients (N = 5) induced CD4⁺ Treg proliferation, with the highest increase triggered by anti-PD1 (*p < 0.05) and the lowest by anti-LAG3. C Treatment of BMMC from MM patients (N = 3) with single agent anti-PD1, anti-OX40, or anti-GITR enhanced (*p < 0.05) proliferation of Treg, which was decreased by combination treatment with checkpoint inhibitor (α-PD1 + α-LAG3) compared to combination with immune agonist (α-OX40 + α-GITR) or single agent treatment.