ArticleProceedings of the National Academy of Sciences of the United States of America2022
MicroRNA-29a attenuates CD8 T cell exhaustion and induces memory-like CD8 T cells during chronic infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 19 citations in OpenAlex.
- Identification of key genes associated with T cell exhaustion in HIV infection based on transcriptomic data.Virology journal · 2026Article
- Exercise‑induced extracellular vesicle microRNA regulates physiological function (Review).Molecular medicine reports · 2026Review
- MicroRNA-29a enhances and preserves stem-like CD8 T cell differentiation by regulating master epigenetic circuits of exhaustion.bioRxiv : the preprint server for biology · 2026Article
- An efficient framework to decipher microRNA regulatory programs applied to T cells.Genes and immunity · 2025Article
- The costimulatory molecule ICOS limits memory-like properties and function of exhausted PD-1Immunity · 2025Article
- Article
- Memory-promoting function of miR-379-5p attenuates CD8Journal for immunotherapy of cancer · 2025Article
- NAPTUNE: nucleic acids and protein biomarkers testing via ultra-sensitive nucleases escalation.Nature communications · 2025Article
- Epigenetic regulation of CD8Frontiers in immunology · 2025Review
- Bioinformatics-based Investigation to Unveiling The miRNA-Immunity Axis in The Tumor Microenvironment of Pancreatic Cancer.F1000Research · 2025Article
- Unraveling the interplay of CD8 + T cells and microRNA signaling in cancer: implications for immune dysfunction and therapeutic approaches.Journal of translational medicine · 2024Review
- Identification of miR-29a as a novel biomarker for lumpy skin disease virus exposure in cattle.Virulence · 2024Article
- Local TSH/TSHR signaling promotes CD8Cancer communications (London, England) · 2024Article
- HIF-2α-dependent induction of miR-29a restrains TNature communications · 2024Article
- Targeting the epigenome to reinvigorate T cells for cancer immunotherapy.Military Medical Research · 2023Review
- The Crossroads of Cancer Epigenetics and Immune Checkpoint Therapy.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Review
- Controlling viral inflammatory lesions by rebalancing immune response patterns.Frontiers in immunology · 2023Review
- Exhausted T cells hijacking the cancer-immunity cycle: Assets and liabilities.Frontiers in immunology · 2023Review
- MicroRNA-29a attenuates CD8 T cell exhaustion and induces memory-like CD8 T cells during chronic infection.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
24 authors at 4 institutions in 1 country.
Funding
Abstract
CD8 T cells mediate protection against intracellular pathogens and tumors. However, persistent antigen during chronic infections or cancer leads to T cell exhaustion, suboptimal functionality, and reduced protective capacity. Despite considerable work interrogating the transcriptional regulation of exhausted CD8 T cells (TEX), the posttranscriptional control of TEX remains poorly understood. Here, we interrogated the role of microRNAs (miRs) in CD8 T cells responding to acutely resolved or chronic viral infection and identified miR-29a as a key regulator of TEX. Enforced expression of miR-29a improved CD8 T cell responses during chronic viral infection and antagonized exhaustion. miR-29a inhibited exhaustion-driving transcriptional pathways, including inflammatory and T cell receptor signaling, and regulated ribosomal biogenesis. As a result, miR-29a fostered a memory-like CD8 T cell differentiation state during chronic infection. Thus, we identify miR-29a as a key regulator of TEX and define mechanisms by which miR-29a can divert exhaustion toward a more beneficial memory-like CD8 T cell differentiation state.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.