ArticleExperimental and therapeutic medicine2014
Regulatory effect of microRNA-135a on the Th1/Th2 imbalance in a murine model of allergic rhinitis.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- MicroRNAs as current diagnostic biomarkers and potential therapeutic targets in allergic and non-allergic rhinitis - A functional characterization.Current allergy and asthma reports · 2026Review
- MicroRNAs-Are They Possible Markers of Allergic Diseases and Efficient Immunotherapy?International journal of molecular sciences · 2026Review
- LncRNA PELATON regulates Th2 cell differentiation by miR-10b-5p/GATA3 axis in allergic rhinitis.The World Allergy Organization journal · 2025Article
- Atractylenolide I alleviates the experimental allergic response in mice by suppressing TLR4/NF-kB/NLRP3 signalling.Open life sciences · 2025Article
- Expression of serum miR-135a in patients with allergic rhinitis and its relationship with Treg/Th17 balance.The Kaohsiung journal of medical sciences · 2025Article
- The Role of Noncoding RNA in Airway Allergic Diseases through Regulation of T Cell Subsets.Mediators of inflammation · 2022Review
- Protective effect of miR-138-5p inhibition modified human mesenchymal stem cell on ovalbumin-induced allergic rhinitis and asthma syndrome.Journal of cellular and molecular medicine · 2021Article
- Modulation of Immune Response toFrontiers in cellular and infection microbiology · 2021Article
- MicroRNA-466a-3p attenuates allergic nasal inflammation in mice by targeting GATA3.Clinical and experimental immunology · 2019Article
- MicroRNAs: Potential Biomarkers and Targets of Therapy in Allergic Diseases?Archivum immunologiae et therapiae experimentalis · 2019Review
- Dendritic Cell-Mediated Th2 Immunity and Immune Disorders.International journal of molecular sciences · 2019Review
- Chinese Society of Allergy Guidelines for Diagnosis and Treatment of Allergic Rhinitis.Allergy, asthma & immunology research · 2018Review
- MicroRNA-let-7e regulates the progression and development of allergic rhinitis by targeting suppressor of cytokine signaling 4 and activating Janus kinase 1/signal transducer and activator of transcription 3 pathway.Experimental and therapeutic medicine · 2018Article
- Correlation of microRNA profiles with disease risk and severity of allergic rhinitis.International journal of clinical and experimental pathology · 2018Article
- MicroRNA-20b promotes the accumulation of CD11b+Ly6G+Ly6CCentral-European journal of immunology · 2017Article
- Intranasal Administration of Lentiviral miR-135a Regulates Mast Cell and Allergen-Induced Inflammation by Targeting GATA-3.PloS one · 2015Article
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11 authors.
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Abstract
Allergic rhinitis (AR) is primarily caused by a T helper cell (Th)1/Th2 imbalance. In a murine AR model of a previous study, the serum ovalbumin (OVA)-sIgE concentration was high, whereas microRNA (miR)-135a was lowly expressed in the nasal mucosa. The abnormal expression pattern of miR-135a coincided with highly expressed endogenous factors, including GATA binding protein (GATA)-3 and interleukin (IL)-4, and lowly expressed factors, including T-box expressed in T cells (T-bet) and interferon (IFN)-γ. We hypothesized that miR-135a may play an important role in immune regulation in AR mice. In the present study, AR was induced by OVA in the mice. Two groups of the AR mice were treated with a miR-135a mimic and a mimic control, respectively. The serum and nasal mucosa were collected for analysis. Following miR-135a application, the serum OVA-sIgE concentration was significantly reduced. In the nasal mucosa, the expression levels of miR-135a were higher, the mRNA and protein expression levels of GATA-3 and IL-4 were lower, and the expression levels of T-bet and IFN-γ were higher. The miR-135a corrected the Th1/Th2 imbalance in the AR mice. Findings of this study may provide a basis for novel genetic treatments in addressing allergic diseases.
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