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. 2022 Dec 23;20:615. doi: 10.1186/s12967-022-03807-8

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© The Author(s) 2022

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 6 — Schematic illustration of the mechanism by which IPD enhances immunotherapy response. Th2-mediated immunity suppresses ICB response by inhibiting the infiltration and cytotoxic activity of CD8⁺ T cell and reshaping the global immune landscape including decreasing the infiltration of effector CD4⁺ T cell and recruiting immunosuppressive cells such as MDSCs and M2-macrophage in tumor microenvironment. Targeting Th2 immunity by IPD can reverse the immunosuppressive microenvironment, thereby improve ICB response and inhibit tumor growth of breast cancer