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Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy. [TCR]

ABSTRACT: Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy. [TCR]

PROVIDER: PRJNA674781 | ENA |

REPOSITORIES: ENA

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Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy. [RNA-Seq]

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Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy.

Project description:Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy.

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Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy. [TCR]

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Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy. [RNA-Seq]

Project description:Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy. [RNA-Seq]

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Tumor-infiltrating mast cells are associated with resistance to anti-PD-1 therapy.

Project description:Anti-PD-1 therapy is used as a front-line treatment for many cancers, but mechanistic insight into this therapy resistance is still lacking. Here we generate a humanized (Hu)-mouse melanoma model by injecting fetal liver-derived CD34+ cells and implanting autologous thymus in immune-deficient NOD-scid IL2Rγnull (NSG) mice. Reconstituted Hu-mice are challenged with HLA-matched melanomas and treated with anti-PD-1, which results in restricted tumor growth but not complete regression. Tumor RNA-seq, multiplexed imaging and immunohistology staining show high expression of chemokines, as well as recruitment of FOXP3+ Treg and mast cells, in selective tumor regions. Reduced HLA-class I expression and CD8+/Granz B+ T cells homeostasis are observed in tumor regions where FOXP3+ Treg and mast cells co-localize, with such features associated with resistance to anti-PD-1 treatment. Combining anti-PD-1 with sunitinib or imatinib results in the depletion of mast cells and complete regression of tumors. Our results thus implicate mast cell depletion for improving the efficacy of anti-PD-1 therapy.

| S-EPMC7804257 | biostudies-literature

Single Cell Sequencing Analysis of Infiltrating Immune Cells in Orthotopically Implanted Liver Cancer in Mice Treated with Isotype or Anti-PD-1 Therapy

Project description:The anti-PD-1 mAb is a type of immunotherapy known to have a significant impact on tumor immune components. In this study, we utilized single-cell RNA sequencing (scRNAseq) to analyze infiltrating immune cells of liver cancer in mice treated with both anti-PD-1 and isotype control.

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [TCR-seq]

Project description:Unlike many other hematologic malignancies, Richter syndrome (RS), an aggressive B cell lymphoma originating from indolent chronic lymphocytic leukemia, is responsive to PD-1 blockade. To discover the determinants of response, we analyzed single-cell transcriptome data generated from 17 bone marrow samples longitudinally collected from 6 RS patients. Response was associated with intermediate exhausted CD8 effector/effector memory T cells marked by high expression of the transcription factor ZNF683, determined to be evolving from stem-like memory cells and divergent from terminally exhausted cells. This signature overlapped with that of tumor-infiltrating populations from PD-1 responsive solid tumors. ZNF683 was found to directly target key T cell genes (TCF7, LMO2, CD69) and impact pathways of T cell cytotoxicity and activation. Analysis of pre-treatment peripheral blood from 10 independent RS PD-1 treated patients, as well as solid tumor PD-1 treated patients, supported an association of ZNF683high T cells with response.

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scRNA-seq comparison of B16-GP33 tumor-infiltrating immune cells from IgG, anti-PD-1, anti-PSGL-1, or combination anti-PD-1 and anti-PSGL-1 treated mice

Project description:We use scRNA-seq to show the differences in tumor-infiltrating immune cells among IgG, anti-PD-1, anti-PSGL-1, and combination anti-PD-1 and anti-PSGL-1 treated mice. We show that anti-PSGL-1 treatment resulted in an increase in neutrophil and T cells, anti-PD-1 treatment resulted in an increase in macrophages, and the combination resulted in an increase in T cells and macrophages when compared to the tumors of IgG treated mice. Additionally, we show that Tregulatory cells are decreased in the tumors of anti-PSGL-1 and combination treated mice. Further, we find that anti-PSGL-1 treated CD8 T cells show upregulation of activation and survival genes, while combination treatment increased effector gene expression in CD8 T cells. Both anti-PSGL-1 treatment and combination treatment increase effector gene expression in CD4 T cells when compared to IgG. This scRNA-seq study shows the impact of IgG, anti-PD-1, anti-PSGL-1, and combination anti-PSGL-1 and anti-PD-1 antibody tteatment on tumor-infiltrating immune cells in B16-GP33 melnoma tumor bearing mice.

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BTLA and PD-1 signals attenuate TCR-mediated gene expression

Project description:T cell coinhibitory immune checkpoints, such as PD-1 or BTLA, are bona fide targets in cancer therapy. Here we used a human T cell reporter line to measure transcriptome changes mediated by PD-1 and BTLA induced signalling. TCR/CD3 stimulation resulted in the upregulation of a large number of genes but also repressed a similar number of transcripts. PD-1 and BTLA signals attenuated transcriptomics changes mediated by TCR/CD3 signalling: upregulated genes tended to be suppressed and the expression of a significant number of downregulated genes was higher when PD-1 or BTLA signalling took place. BTLA was a significantly stronger attenuator of TCR/CD3 induced transcriptome changes than PD-1. A strong overlap between genes that were regulated indicated quantitative rather than qualitative differences between these receptors. In line with their function as attenuator of TCR/CD3 mediated changes we found strongly regulated genes to be prime targets of PD-1 and BTLA signalling.

2024-05-27 | GSE239586 | GEO

Mast cells decrease efficacy of anti-angiogenic therapy by secreting matrix-degrading granzyme B

Project description:Resistance towards anti-angiogenic therapy (AAT) still represents a substantial clinical challenge. We report here that tumor-infiltrating mast cells (MC) are powerful mediators decreasing efficacy of AAT in mice and cancer patients. They act in a cell-extrinsic manner by secreting granzyme B, which liberates pro-angiogenic mediators from the extracellular matrix. In addition, MC also diminish efficacy of anti-angiogenic agents in a cell-autonomous way, which can be blocked by the mast cell degranulation inhibitor cromolyn. Our findings are relevant in humans because patients harboring higher numbers of MC in their tumors have an inferior outcome after anti-angiogenic treatment in the Gepar Quinto randomized Phase 3 clinical trial. Thus, MC-targeting might represent a novel promising approach to increase efficacy of AAT.

2017-09-15 | GSE89395 | GEO

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