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Publication

Targeting EZH2 Reprograms Intratumoral Regulatory T Cells to Enhance Cancer Immunity.

David Wang | Jason Quiros | Kelly Mahuron | Chien-Chun Pai | Valeria Ranzani | Arabella Young | Stephanie Silveria | Tory Harwin | Arbi Abnousian | Massimiliano Pagani | Michael D Rosenblum | Frederic Van Gool | Lawrence Fong | Jeffrey A Bluestone | Michel DuPage
Cell reports | 2018

Regulatory T cells (Tregs) are critical for maintaining immune homeostasis, but their presence in tumor tissues impairs anti-tumor immunity and portends poor prognoses in cancer patients. Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8+ and CD4+ effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.

Pubmed ID: 29898397

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Associated grants

  • Agency: NIAMS NIH HHS, United States
    Id: DP2 AR068130
  • Agency: NIAID NIH HHS, United States
    Id: R01 AI046643
  • Agency: NCI NIH HHS, United States
    Id: T32 CA128583

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