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Spatial regulation of CD8+ T cells at the HLA-E-NKG2A axis drives HIV persistence in Lymph Node B Cell Follicles

GSE297327 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2025/08/26 Platform GPL18573
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 18 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Homo sapiens (human)
Samples
18 samples: 6 × Bulk CD8 Lymph Node ATAC-Seq vs 5 × Bulk CD8 Peripheral Blood ATAC-Seq vs 4 × Bulk CD8 Peripheral Blood RNA-Seq vs 3 × Bulk CD8 Lymph Node RNA-SeqGroups 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)
B cell follicles (BCF) in the lymph node are a major sanctuary for HIV reservoirs. Immune regulatory mechanisms hindering cytolytic CD8+ responses at these sites, are poorly characterized, likely enabling HIV persistence. Spatial transcriptomics and high- dimensional histocytometry were used to define CD8+ T cell function and immune regulation in LN follicles of people Living with HIV (PLWH), at various stages of ART- treatment.
Read the full summary ↓
Histocytometry demonstrated that CD8+ T cells infiltrating BCF mostly lacked granzyme B expression, coinciding with reduced chromatin access at cytolytic gene loci in dissociated lymph node cells. Spatial transcriptomics confirmed the immune regulatory microenvironment of HIV-infected BCF, particularly exhibiting upregulation of HLA-E. Additional FACS analysis identified a subset of LN CD8+ T cells expressing the NKG2A-interacting partner of HLA-E, with reduced granzyme B expression. These findings reveal regulation of follicular CD8+ T cells at the HLA-E- NKG2A axis as a key mechanism for HIV immune evasion.
This dataset
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.

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 GSE297327_RAW.tar (it can run to tens of gigabytes).

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.

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1263523 and SRA study SRP585619. Searching any of these in the dataset finder brings you back here.

Study design
6 × Bulk CD8 Lymph Node ATAC-Seq vs 5 × Bulk CD8 Peripheral Blood ATAC-Seq vs 4 × Bulk CD8 Peripheral Blood RNA-Seq vs 3 × Bulk CD8 Lymph Node RNA-Seq

Supports a between-group comparison across 18 samples.

How we read this: 4 replicated groups read from 18 sample titles; they account for 18 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
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