ArticleJournal of immunology (Baltimore, Md. : 1950)2015
miR-182 is largely dispensable for adaptive immunity: lack of correlation between expression and function.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers, 1 of them a synthesis that pooled it.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Protection of macrophages from intracellular pathogens by miR-182-5p mimic-a gene expression meta-analysis approach.The FEBS journal · 2018Pooled it
- MicroRNAs as Biomarkers for the Diagnosis and Prognosis of Different Diseases and Cancer.Experientia supplementum (2012) · 2026Review
- Article
- Ataxia Telangiectasia Mutated and MSH2 Control Blunt DNA End Joining in Ig Class Switch Recombination.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- MicroRNA-183/96/182 cluster in immunity and autoimmunity.Frontiers in immunology · 2023Review
- miR-182 targeting reprograms tumor-associated macrophages and limits breast cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Deletion of microRNA-183-96-182 Cluster in Lymphocytes Suppresses Anti-DsDNA Autoantibody Production and IgG Deposition in the Kidneys in C57BL/6-FasFrontiers in genetics · 2022Article
- miRNA-Mediated Control of B Cell Responses in Immunity and SLE.Frontiers in immunology · 2021Review
- Mutation Screening in the miR-183/96/182 Cluster in Patients With Inherited Retinal Dystrophy.Frontiers in cell and developmental biology · 2020Article
- AID Phosphorylation Regulates Mismatch Repair-Dependent Class Switch Recombination and Affinity Maturation.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation.Cell stem cell · 2019Article
- The B Cell Activation-Induced miR-183 Cluster Plays a Minimal Role in Canonical Primary Humoral Responses.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- The E3 ubiquitin ligase Itch is required for B-cell development.Scientific reports · 2019Article
- miR-212 and miR-132 Are Downregulated in Neurally Derived Plasma Exosomes of Alzheimer's Patients.Frontiers in neuroscience · 2019Article
- Decreased microRNA-182-5p helps alendronate promote osteoblast proliferation and differentiation in osteoporosis via the Rap1/MAPK pathway.Bioscience reports · 2018Article
- Mapping the Pax6 3' untranslated region microRNA regulatory landscape.BMC genomics · 2018Article
- Cutting Edge: The Transcription Factor Sox2 Regulates AID Expression in Class-Switched B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Absence of miR-182 Augments Cardiac Allograft Survival.Transplantation · 2017Article
- Nogo-C regulates cardiomyocyte apoptosis during mouse myocardial infarction.Cell death & disease · 2016Article
- Antigen specific immune response in Chlamydia muridarum genital infection is dependent on murine microRNAs-155 and -182.Oncotarget · 2016Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
MicroRNA (miR)-mediated regulation of protein abundance is a pervasive mechanism of directing cellular processes. The well-studied and abundant miR-182 has previously been implicated in many aspects of T cell function, DNA repair, and cancer. In this study, we show that miR-182 is the most highly induced miR in B cells undergoing class-switch recombination. To elucidate the requirement of miR-182 in lymphocyte function, we extensively characterized mice with a targeted deletion of Mir182. We show that despite its dramatic induction, loss of miR-182 has minimal impact on B cell development, the ability of B cells to undergo class-switch recombination ex vivo and to undergo Ag-driven affinity maturation in vivo. Furthermore, in striking contrast to knockdown studies that demonstrated the requirement of miR-182 in T cell function, miR-182-deficient mice display no defect in T cell development and activation. Finally, we show that T cell-dependent immune response to experimental Listeria monocytogenes infection is intact in miR-182-deficient mice. We conclude that, contrary to previous studies, miR-182 does not play a significant role in all measured aspects of mouse adaptive immunity. This striking absence of a phenotype highlights the lack of correlation between expression pattern and functional requirement, underscores the limitations of using knockdown approaches to assess miR requirements, and suggests that miR networks may compensate for the chronic loss of specific miRs.
Indexed as
Identifiers
What OpenQuestion holds
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.