GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE304nnn/GSE304995/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE304995GEOGSEfalseHIV-1 reprograms CD4 T cell responses by impairing antigen-specific communication with dendritic cellsHIV-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.2026/08/07GSE304995GSM9160752GSM9160751GSM9160754GSM9160753GSM9160756GSM9160755GSM9160758GSM916075724247304995Mus musculus