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Omics · study · 2026

Gene Expression Profiling of Recipient Immune Cells Induced by 7 × 19 CAR-T Cell Dosing in a Syngeneic Mouse Model [scRNA-Seq]

Listed in NCBI GEO

Chimeric antigen receptor (CAR)-T cell therapy is effective for hematologic malignancies; however, the response of solid tumors is limited because of the immunosuppressive tumor microenvironment, antigen heterogeneity, and lack of persistence of transferred T cells.

Description

To overcome these challenges, CAR-T cells expressing interleukin-7 and chemokine (C-C motif) ligand 19 (7 × 19 CAR-T) were generated to achieve potent antitumor efficacy through the recruitment and proliferation of CAR-T cells and endogenous immune cells.

To elucidate the underlying mechanism of 7 × 19 CAR-T cells against solid tumors, we analyzed the cellular composition and gene expression profiles of host immune cells following CAR-T cell infusion in a murine solid tumor model. Antihuman CD20 7 × 19 CAR-T cells were prepared using Thy 1.1 congenic mice and administered to C57BL/6N mice bearing subcutaneous MC38 tumors expressing human CD20. The tumors were harvested 4 days postinfusion to capture early immune responses before overt tumor regression.

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CD90.1- recipient immune cells were subjected to flow cytometry analysis, and transcriptomics changes were determined using AmpliSeq and single-cell RNA seq. An increase in recipient CD8+ T cells and macrophages was observed in the tumor of mice treated with 7 × 19 CAR-T cells, but not with conventional CAR-T. The expression of chemokines and genes associated with the inflammatory pathway was upregulated only in recipient immune cells of the 7 × 19 CAR-T-treated mice.

Single-cell RNA-seq analysis revealed upregulation of pro-inflammatory genes and chemokines in the dendritic cell and monocyte/macrophage populations. These results indicate that 7 × 19 CAR-T cells initiate the early recruitment and activation of host immune cells, which contributes to their superior antitumor activity compared with conventional CAR-T cells.

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Life Sciences
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Cancer 65% · RNA sequencing 65% · Single-cell RNA sequencing 65%
Provenance · 1 source records, 10 field assertions
SourceKeyLast seenRaw
NCBI GEOGSE31488512 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[disease].local:disease:cancerenrichment · NCBI GEOkeyword-concept-rules@1.0.0title+description (65%)
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
concepts[modality].local:modality:rna-seqenrichment · NCBI GEOkeyword-concept-rules@1.0.0title+description (65%)
concepts[modality].local:modality:single-cell-rna-seqenrichment · NCBI GEOkeyword-concept-rules@1.0.0title+description (65%)
concepts[organism].NCBITaxon:10090source · NCBI GEOconnector:ncbi_geo@1.0.0/taxon
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title