bioRxivCancer BiologyPreprint
Epigenetic therapy remodels the immune synaptic cytoskeleton to potentiate cancer susceptibility to γδ T cells
R. R. Weng, H.-H. Lu, C.-T. Lin, C.-C. Fan, R.-S. Lin, T.-C. Huang, S.-Y. Lin, Y.-J. Huang, Y.-H. Juan, Y.-C. Wu, Z.-C. Hung, C. Liu, X.-H. Lin, W.-C. Hsieh, T.-Y. Chiu, J.-C. Liao, Y.-L. Chiu, S.-Y. Chen, C.-J. Yu, H.-C. Tsai
Abstract
{gamma}{delta} T cells are a distinct subgroup of T cells that bridge the innate and adaptive immune systems and can attack cancer or virus-infected cells in an MHC-unrestricted manner. Despite its antitumor ability in both autologous and allogeneic settings, earlier trials of adoptive {gamma}{delta} T cell transfer in solid tumors had limited success due to limitations in cell expansion and the lack of a strategy to modulate tumor lytic interactions between {gamma}{delta} T and cancer cells. Here, we show through quantitative surface proteomics and gene enrichment analyses that DNA methyltransferase inhibitors (DNMTis) upregulate multiple surface molecules related to {gamma}{delta} T cell activation in cancer cells. DNMTi treatment of human lung cancer potentiates tumor lysis by ex vivo-expanded {gamma}{delta} T cells using a clinical-grade expansion protocol developed by our team to enrich for the V{delta}1 subset while preserving their antitumor effector functions. Mechanistically, DNMTis enhance immune synapse formation and stabilize the synaptic cleft to facilitate {gamma}{delta} T-mediated tumor lysis. Through integrated analysis of RNA-seq, DNA methylation, and ATAC-seq, we demonstrate that depletion of DNMTs induces coordinated pattern alterations of immune synaptic-cytoskeletal networks at the cancer side of the immune synapse. In addition, single-cell mass cytometry reveals enrichment of polyfunctional {gamma}{delta} T subsets by DNMTis. Combined DNMTi and adoptive {gamma}{delta} T transfer in a mouse lung cancer model offers a significant survival benefit. Consistently, the DNMTi-associated cytoskeleton signature identifies a subset of lung cancer patients with improved survival. Our results demonstrate that epigenetic mechanisms are crucial for cytoskeletal remodeling in cancer to potentiate immune attack and support a combinatorial strategy of DNMTis and {gamma}{delta} T cell-based immunotherapy in lung cancer management. One Sentence SummaryDNA methyltransferase inhibitors potentiate the killing of lung cancer by {gamma}{delta} T cells through remodeling cytoskeletal-immune synaptic networks.
- organism: human
- organism: mouse
- assay: proteomics
- assay: DNA methylation
- assay: ATAC-seq
- assay: bulk RNA-seq
- research focus: cell-cell communication
- research focus: differential expression
- research focus: drug response / drug discovery
- approach: statistical model
- approach: experimental assay
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