ArticleThe Journal of clinical investigation2015
Mature T cell responses are controlled by microRNA-142.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
60 citing papers in PubMed, 84 citations in OpenAlex.
- Article
- POU2F1 Promotes Chemoresistance in Colorectal Cancer Cells via Attenuates the MDR2 Degradation Mediated by PPP1R11 Lactylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Advances in graft-versus-host disease: emerging therapeutic strategies, biomarker discoveries, and innovative treatment approaches.Frontiers in immunology · 2026Review
- Prediction of transplant rejection using non-coding RNAs.Molecular biology reports · 2025Review
- MicroRNA-142 improves IL1RAP CAR-T cell activity in acute myeloid leukemia.Journal of hematology & oncology · 2025Article
- miR-142 deficit in T cells during blast crisis promotes chronic myeloid leukemia immune escape.Nature communications · 2025Article
- MicroRNA-142 regulates gut associated lymphoid tissues and group 3 innate lymphoid cells.Mucosal immunology · 2025Article
- The role of microRNAs in primary Sjögren's disease: deciphering regulatory networks and assessing current therapeutic perspectives.Frontiers in immunology · 2025Review
- MicroRNA expression signature as a biomarker in the diagnosis of nodal T-cell lymphomas.Cancer cell international · 2024Article
- miR-142: A Master Regulator in Hematological Malignancies and Therapeutic Opportunities.Cells · 2023Review
- Acquired miR-142 deficit in leukemic stem cells suffices to drive chronic myeloid leukemia into blast crisis.Nature communications · 2023Article
- A gain-of-function mutation in microRNA 142 is sufficient to cause the development of T-cell leukemia in mice.Cancer science · 2023Article
- A panel of blood-based circulatory miRNAs with diagnostic potential in patients with psoriasis.Frontiers in medicine · 2023Article
- Opposing functions of circadian protein DBP and atypical E2F family E2F8 in anti-tumor Th9 cell differentiation.Nature communications · 2022Article
- Insights into mechanisms of graft-versus-host disease through humanised mouse models.Bioscience reports · 2022Review
- Rearrangement of T Cell genome architecture regulates GVHD.iScience · 2022Article
- MicroRNA-31 regulates T-cell metabolism via HIF1α and promotes chronic GVHD pathogenesis in mice.Blood advances · 2022Article
- microRNA-142 guards against autoimmunity by controlling Treg cell homeostasis and function.PLoS biology · 2022Article
- Review
- Circulating miR-455-3p, miR-5787, and miR-548a-3p as potential noninvasive biomarkers in the diagnosis of acute graft-versus-host disease: a validation study.Annals of hematology · 2021Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
T cell proliferation is critical for immune responses; however, the molecular mechanisms that mediate the proliferative response are poorly understood. MicroRNAs (miRs) regulate various molecular processes, including development and function of the immune system. Here, utilizing multiple complementary genetic and molecular approaches, we investigated the contribution of a hematopoietic-specific miR, miR-142, in regulating T cell responses. T cell development was not affected in animals with a targeted deletion of Mir142; however, T cell proliferation was markedly reduced following stimulation both in vitro and in multiple murine models of graft-versus-host disease (GVHD). miR-142-deficient T cells demonstrated substantial cell-cycling defects, and microarray and bioinformatics analyses revealed upregulation of genes involved in cell cycling. Moreover, 2 predicted miR-142 target genes, the atypical E2F transcription factors E2f7 and E2f8, were most highly upregulated in miR-142-deficient cells. Clustered regularly interspaced short palindromic repeat interference-mediated (CRISPRi-mediated) silencing of E2F7 and E2F8 in miR-142-deficient T cells ameliorated cell-cycling defects and reduced GVHD, and overexpression of these factors in WT T cells inhibited the proliferative response. Together, these results identify a link between hematopoietic-specific miR-142 and atypical E2F transcription factors in the regulation of mature T cell cycling and suggest that targeting this interaction may be relevant for mitigating GVHD.
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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.