Pharmacological and Genetic Modulation of IL-32 Expression in Intestinal Epithelial Cells

A 650.9 KB PDF research article by Etiene Moreira Gabriel, last updated in May 2026, details an experimental study on HIV-1 latency. The work identifies IL-22, ATRA, and RGZ as novel regulators of IL-32 expression in TNF-primed intestinal epithelial cells. Results demonstrate that modulating IL-32 expression does not significantly impact HIV-1 outgrowth from co-cultured CD4+ T-cells of ART-treated individuals.

Use Cases

• Analyzing the effects of cytokine (TNF, IL-22, IL-26) and pharmacological (ATRA, RGZ) treatments on IL-32 expression based on RT-PCR/ELISA results.
• Investigating the impact of CRISPR/Cas9-mediated IL32 knockout on IEC transcriptional profiles based on whole-genome RNA-Sequencing data.
• Evaluating the role of IEC-T-cell crosstalk in HIV-1 reservoir reactivation based on viral outgrowth assay (VOA) and p24 measurements.
• Studying the relationship between IL-32 expression and HIV-1 disease progression markers as suggested in the background.

Strengths

• The dataset is a detailed, peer-reviewed research article describing specific experimental methods including CRISPR/Cas9 editing and RNA-Seq.
• It provides concrete findings on the effects of multiple modulators (IL-22, ATRA, RGZ) on IL-32β/γ/ϵ isoforms.
• The study uses primary cells from ART-treated people with HIV-1 for the viral outgrowth assays.

Limitations

• The primary data format is a PDF document; underlying raw experimental data (e.g., RNA-Seq reads, flow cytometry files) are not directly accessible.
• Row count and column-level documentation for any underlying tabular data are unknown.
• The dataset's scope is limited to the specific in vitro co-culture model described.

Provenance

Source

figshare

Collection Method

Experimental laboratory research involving cell culture, gene editing, cytokine stimulation, and viral outgrowth assays.

Freshness

Last updated 2026-05-26 07:48:58