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Updated: Jul 27, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
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Published on: August 23, 2019

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PPARδ inhibition blocks the induction and function of tumor-induced IL-10

Chen Chen1,2,3, Jianan Ma1,2, Chenchen Pi1,2

  • 1Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, The First Hospital of Jilin University, Changchun, Jilin, China.

Cell Discovery
|June 8, 2023
PubMed

IL-10+ regulatory B cells (Bregs) play a significant role in cancer immunotherapy and their presence is an indicator of negative outcome. We found that PPARδ is significantly upregulated in tumor-induced IL-10+ Bregs with a phenotype of CD19+CD24hiIgDlo/-CD38lo or CD19+CD24hiIgDlo/-CD38hi in both mice and humans, and the level of PPARδ expression was correlated with their potential to produce IL-10 and to inhibit T cell activation. Genetic inactivation of PPARδ in B cells impaired the development and function of IL-10+ B cells, and treatment with PPARδ inhibitor diminished the induction of IL-10+ Bregs by tumor and CD40 engagement. Importantly, immunotherapy with anti-CD40 or anti-PD1 antibody achieved a markedly improved outcome in tumor-bearing mice with PPARδ deficiency in B cells or treated with PPARδ inhibitor. This study shows that PPARδ is required for the development and function of IL-10+ Bregs, providing a new and effective target for selectively blocking Bregs and improving antitumor immunotherapy.

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