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Clonal spreading of tumor-infiltrating T cells underlies the durable antitumor effects of PD-1 blockade and anti-CD4 monoclonal antibody

ABSTRACT: Clonal spreading of tumor-infiltrating T cells underlies the durable antitumor effects of PD-1 blockade and anti-CD4 monoclonal antibody

PROVIDER: PRJNA814218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18277205.fastq.gz	Fastqsanger.gz
	SRR18277206.fastq.gz	Fastqsanger.gz
	SRR18277207.fastq.gz	Fastqsanger.gz
	SRR18277208.fastq.gz	Fastqsanger.gz
	SRR18277209.fastq.gz	Fastqsanger.gz

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Clonal spreading of tumor-infiltrating T cells underlies the durable antitumor effects of PD-1 blockade and anti-CD4 monoclonal antibody: Bulk TCR sequencing

Project description:The repertoire of tumor-infiltrating T cells is a novel perspective to characterize effective anti-tumor T cell responses. Previous studies reported that the oligoclonal expansion in tumor T-cell repertoire is associated with anti-tumor effects. However, the contribution of the expansion of diverse T-cell clones remained unclear. We demonstrated that the polyclonal fraction of tumor-reactive T-cell repertoire consisting of relatively minor clones, increased in tumor-bearing mice treated with anti-PD-L1 or anti-CD4 monoclonal antibodies (mAbs), while the oligoclonal fraction consisting of major clones was unchanged. Moreover, the polyclonal fraction was enriched with progenitor exhausted T cells, essential for a durable anti-tumor response, and more dependent on CCR7+ migratory dendritic cells, responsible for priming tumor-reactive T cells in the tumor-draining lymph node (dLN). These results proposed that the expansion of diverse tumor-reactive clones, “clonal spreading,” is an important mechanism by which anti-PD-L1 and anti-CD4 treatments exert robust and durable anti-tumor T-cell responses.

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Clonal spreading of tumor-infiltrating T cells underlies the durable antitumor effects of PD-1 blockade and anti-CD4 monoclonal antibody: Bulk TCR sequencing

Project description:Clonal spreading of tumor-infiltrating T cells underlies the durable antitumor effects of PD-1 blockade and anti-CD4 monoclonal antibody: Bulk TCR sequencing

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Clonal spreading of tumor-infiltrating T cells underlies the durable antitumor effects of PD-1 blockade and anti-CD4 monoclonal antibody

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-05-11 | GSE198211 | GEO

HDACi promotes inflammatory remodeling of the tumor microenvironment to enhance epitope spreading and antitumor immunity

Project description:Adoptive cell therapy (ACT) with tumor-specific memory T cells has shown increasing efficacy in regressing solid tumors. However, tumor antigen heterogeneity represents a longitudinal challenge for durable clinical responses due to the therapeutic selective pressure for immune escape variants. Here, we demonstrate that delivery of class I histone deacetylase inhibitor, MS-275, promotes sustained tumor regression by synergizing with ACT in a coordinated manner to enhance cellular apoptosis. We find that MS-275 alters the tumor inflammatory landscape to support antitumor immunoactivation through the recruitment and maturation of cross-presenting CD103+ and CD8+ dendritic cells and depletion of regulatory T cells. Activated endogenous CD8+ T cell responses against non-target tumor antigens was critically required for the prevention of tumor recurrence. Importantly, MS-275 alters the immunodominance hierarchy by directing epitope spreading towards endogenous retroviral tumor-associated antigen, p15E. Our data suggest that MS-275 multi-mechanistically improves epitope spreading to promote long-term clearance of solid tumors.

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Dynamic magneto-mechanical force in lysosomes instructs durable macrophage repolarization for antitumor immunity.

Project description:Mechanical forces are the emerging physical cue to regulate biochemical signals of immune cells for antitumor immunity. Here, we develop a magneto-mechanical force-triggered lysosomal membrane permeabilization (MagLMP) strategy to dictate durable macrophage repolarization, which leads to dynamic damage of lysosomal membrane via the finely tuned torque-induced vortex. We found that the MagLMP could activate M1-like macrophage repolarization, followed by the mounting of antitumor immunity. Together, we establish an intracellular mechanical strategy to dynamically manipulate innate immune responses in vivo and provide the tool for durable immunotherapy through organelle mechanotransduction.

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Project description:The induction of an antitumor CD4+ T helper response is essential for the efficacy of therapeutic cancer vaccines. However, few vaccines are specifically designed to target CD4+ T cells in human cancers. Here, we characterize the immune mechanisms of UCPVax, a helper peptide vaccine derived from telomerase. Ex vivo immune profiling of peripheral blood from 60 patients with advanced lung cancer reveals that UCPVax selectively activates CD4+ T cells in vivo across a broad HLA-DR restriction. The vaccine elicits a synergistic immune triad including cytokine-polyfunctional CD4+ Th1 cells, epitope spreading, and antibody response, contributing to effective tumor control. Single-cell analysis further demonstrates that UCPVax drives CD4+ T cells toward effector-memory and cytolytic differentiation. Thus, the vaccine-induced CD4+T cells trigger a broad and durable antitumor immunity. These findings highlight UCPVax as an off-the-shelf helper platform to enhance therapeutic cancer vaccine efficacy.

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UCPVax, a CD4 helper peptide vaccine induces polyfunctional Th1 cells, antibody response and epitope spreading to improve antitumor immunity [TCR-seq]

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Profiling of spreading- coupled protein tyrosine phosphorylation

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