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HIV-1 reprograms CD4 T cell responses by impairing antigen-specific communication with dendritic cells

GSE304995 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2026/08/07 Platform GPL24247
Summary
HIV-1 infection causes general dysfunction of adaptive immune cells that persists even under therapy but the underlaying mechanisms remain elusive. Antigen-specific interactions of the main target cells of HIV, CD4 T cells, with dendritic cells (DCs) orchestrate global T cell responses and convey help to CD8 T cells. Here we report that HIV-1, by virtue of its pathogenesis factor Nef, impairs activation and transcriptionally reprograms CD4 T cells to dampen Th1 differentiation in response to antigen-specific stimulation by DCs. These alterations also disrupt functional communication to DCs to reduce DC activation and limit Th1 helper cytokine production. Mechanistically, Nef achieves this modulation of antigen-specific CD4 T cell function by reducing T cell surface levels of CD4. These results define modulation of CD4 T cell-DC communication as pathogenic principle by which HIV-1 disrupts adaptive immunity and emphasize the direct role of CD4 in immune cell communication.
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Direct links to NCBI, no account and no request form: the whole study as GSE304995_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 8 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1303660 and SRA study SRP607663. Searching any of these in the dataset finder brings you back here.

Study design
8 × OT-II.2 CD4 T cell-BMDC co-culture_sublib

Supports a between-group comparison across 8 samples.

1 replicated groups read from 8 sample titles; they account for 8 of them. Check it against the sample list below before relying on it.

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