ArticleJCI insight2018
A systems immunology approach identifies the collective impact of 5 miRs in Th2 inflammation.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Interplay between microRNAs and TGF-β signaling in T cells: implications for Th9 differentiation and immune pathogenesis.Frontiers in immunology · 2026Review
- miRNA-146-a, miRNA-21, miRNA-143, miRNA-29-b and miRNA-223 as Potential Biomarkers for Atopic Dermatitis.Clinics and practice · 2025Article
- Vitamin D exerts endogenous control over TiScience · 2025Article
- Fine-tuning levels of filamins a and b as a specific mechanism sustaining Th2 lymphocyte functions.Nature communications · 2024Article
- The Roles of MicroRNAs in Asthma and Emerging Insights into the Effects of Vitamin DNutrients · 2024Review
- Studies on the role of non-coding RNAs in controlling the activity of T cells in asthma.Non-coding RNA research · 2023Review
- Effects of crocin on T-bet/GATA-3 ratio, and miR-146a and miR-106a expression levels in lung tissue of ovalbumin-sensitized mice.Iranian journal of basic medical sciences · 2022Article
- Spotlight on microRNAs in allergy and asthma.Allergy · 2021Review
- Predicting miRNA-based disease-disease relationships through network diffusion on multi-omics biological data.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic asthma is a chronic inflammatory disease dominated by a CD4+ T helper 2 (Th2) cell signature. The immune response amplifies in self-enforcing loops, promoting Th2-driven cellular immunity and leaving the host unable to terminate inflammation. Posttranscriptional mechanisms, including microRNAs (miRs), are pivotal in maintaining immune homeostasis. Since an altered expression of various miRs has been associated with T cell-driven diseases, including asthma, we hypothesized that miRs control mechanisms ensuring Th2 stability and maintenance in the lung. We isolated murine CD4+ Th2 cells from allergic inflamed lungs and profiled gene and miR expression. Instead of focusing on the magnitude of miR differential expression, here we addressed the secondary consequences for the set of molecular interactions in the cell, the interactome. We developed the Impact of Differential Expression Across Layers, a network-based algorithm to prioritize disease-relevant miRs based on the central role of their targets in the molecular interactome. This method identified 5 Th2-related miRs (mir27b, mir206, mir106b, mir203, and mir23b) whose antagonization led to a sharp reduction of the Th2 phenotype. Overall, a systems biology tool was developed and validated, highlighting the role of miRs in Th2-driven immune response. This result offers potentially novel approaches for therapeutic interventions.
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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.