GEO series

Cannabinoid Receptor 2 Agonists Attenuate HIV Replication and Inflammatory Activation in HIV-infected Myeloid Cells

GSE250616 Homo sapiens (human) RNA-seq (gene expression) 16 samples Submitted 2025/01/22 Platform GPL20301

At a glance

RNA-seq (gene expression) · human · 16 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: 16 samples: 16 samples, each with a distinct title — no replicated groupsGroups 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.
Paper: Differential Effects of Cannabinoid Receptor 2 Agonists on HIV Replication and Inflammatory Activation in Monocyte-Derived Macrophages and Induced Pluripotent Stem Cell-Derived MicrogliaJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025

Summary (written by the submitters)

Emerging evidence suggests brain-resident myeloid cells, including macrophages and microglia, provide a reservoir for HIV infection in the central nervous system (CNS), and their inflammatory activation is a proposed pathogenic mechanism in HIV-associated neurocognitive disorders (HAND). We investigated whether cannabinoid receptor 2 (CB2), an immunomodulatory receptor expressed in myeloid cells, regulates viral replication and inflammation in HIV-infected macrophages and microglia.

Read the full summary ↓

Using the synthetic CB2-specific agonist, JWH-133, we found that CB2 activation reduces HIV replication in primary human monocyte-derived macrophages (MDMs) and human iPSC-derived microglia (iMg) at differing doses, corresponding to the basal expression of CNR2 and related endocannabinoid transcripts in each cell type. Direct CB2 agonism via JWH-133 broadly reduced cytokine release from HIV-infected MDMs, but not iMg. RNA-seq revealed that CB2 agonism primarily altered interferon and integrated stress response pathways in MDMs; homeostatic pathways, including synapse maintenance and phagocytosis, were altered in iMg. Further investigation in iMg found NLRP3 inflammasome activation, but not priming, was reduced by CB2 activation. This study identifies key discrepancies in CB2 response between myeloid cell types and implicates CB2-specific agonists as promising candidates for regulation of HIV-associated neuroinflammation.

Published in

Differential Effects of Cannabinoid Receptor 2 Agonists on HIV Replication and Inflammatory Activation in Monocyte-Derived Macrophages and Induced Pluripotent Stem Cell-Derived Microglia

Starr A, Rathore S, Daniali M et al. · Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology 2025 · PMID 41075102 · doi:10.1007/s11481-025-10254-x

This dataset

Open GSE250616 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 GSE250616_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 PRJNA1054626 and SRA study SRP478976. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41075102) ↗

Study design

16 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 16 sample titles: 16 distinct titles with little repetition. 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

GSM7982921 ND224 MDM, HIV + Veh
GSM7982922 ND224 MDM, Mock + Veh
GSM7982923 ND410 MDM, HIV + JWH-133 1 uM
GSM7982924 ND410 MDM, HIV + Veh
GSM7982925 ND410 MDM, Mock + Veh
GSM7982926 ND607 MDM, HIV + JWH-133 1 uM
GSM7982927 ND607 MDM, HIV + Veh
GSM7982928 ND607 MDM, Mock + Veh
GSM7982929 WT6 iMg, HIV + Veh
GSM7982930 WT6 iMg, Mock + Veh
GSM7982931 WT10 iMg, HIV + JWH-133 1 uM
GSM7982932 WT10 iMg, HIV + Veh
GSM7982933 WT10 iMg, Mock + Veh
GSM7982934 WT14 iMg, HIV + JWH-133 1 uM
GSM7982935 WT14 iMg, HIV + Veh
GSM7982936 WT14 iMg, Mock + Veh

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.