GEO series

Inhibition of programmed cell death-1 in cytotoxic CD8+ T cells exacerbates pressure overload-induced cardiac injury

GSE328788 Homo sapiens (human) RNA-seq (gene expression) 14 samples Submitted 2026/05/22 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 14 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Homo sapiens (human)
Samples: 14 samples: 7 × myocarditis vs 7 × ControlGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.

Summary (written by the submitters)

Background: The use of anti-programmed cell death 1 (PD-1) antibody increases heart failure (HF) risk in cancer patients with pre-existing cardiovascular conditions. However, the underlying mechanism remains incompletely understood.

Read the full summary ↓

Methods: To evaluate the effects of anti-PD-1 antibody on transverse aortic constriction (TAC)-induced cardiac remodeling and HF, anti-PD-1 antibody-treated mice, T cell-, myeloid-, and CD8+ T cell-specific PD-1 knockout (KO) mice, and C-X-C motif chemokine receptor 3 (CXCR3) KO and granzyme B (GZMB) KO mice combined with flow cytometry, western blotting, immunofluorescence staining, pharmacological approaches, and bulk RNA-sequencing analyses were used. Results: Administration of anti-PD-1 antibody, T cell-, or CD8+ T cell-specific PD-1 deletion, but not myeloid-specific PD-1 KO, aggravated TAC-induced cardiomyopathy and HF in mice. Mechanistically, PD-1 blockade or deletion increased myocardial infiltration of CXCR3+ CD8+ T cells, which led to GZMB/perforin-mediated impairment of cardiomyocyte mitochondrial complex I to exacerbate TAC-induced cardiac injury and HF. Notably, TAC-enhanced chemotaxis, between cardiac fibroblasts (CF)-derived CXCL9/CXCL10 and CXCR3+ CD8+ T cells, was a driving force for recruiting CXCR3+ CD8+ T cells under the conditions of PD-1 blockade or deletion. The worsened TAC-induced cardiomyopathy caused by anti-PD-1 antibody or T cell-specific PD-1 deletion was rescued by genetic deletion or pharmacological blockade of GZMB and CXCR3. Conclusions: Anti-PD-1 antibody administration enhances myocardial infiltrated CXCR3+ CD8+ T cells under TAC condition via CXCL9/CXCL10-mediated chemotaxis. These CD8+ T cell-released GZMB impairs mitochondrial complex I and causes cardiomyocytes apoptosis in a perforin-dependent manner, exacerbating TAC-induced cardiomyopathy and HF. CXCL9/CXCL10-CXCR3+ CD8+ T cell axis may represent a promising target for combating anti-PD-1 antibody-associated cardiotoxicity.

This dataset

Open GSE328788 in finder → Find more human RNA-seq datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE328788_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1456524 and SRA study SRP693968. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

7 × myocarditis vs 7 × Control

Supports a between-group comparison across 14 samples.

How we read this: 2 replicated groups read from 14 sample titles; they account for 14 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM9689695 myocarditis 1 myocarditis
GSM9689696 myocarditis 2 myocarditis
GSM9689697 myocarditis 3 myocarditis
GSM9689698 myocarditis 4 myocarditis
GSM9689699 Control 1 Control
GSM9689700 Control 2 Control
GSM9689701 Control 3 Control
GSM9845479 Control 4 Control
GSM9845480 Control 5 Control
GSM9845481 Control 6 Control
GSM9845482 Control 7 Control
GSM9845483 myocarditis 5 myocarditis
GSM9845484 myocarditis 6 myocarditis
GSM9845485 myocarditis 7 myocarditis

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