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MiR-146a overexpression effectively improves experimental allergic conjunctivitis through regulating CD4+CD25-T cells
Yang Yang1, Xiaolong Yin1, Jinglin Yi2
1Department of Pediatric Ophthalmology, The Second Affiliated Hospital of Nanchang University, Nanchang, 330006, People's Republic of China.
Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|August 17, 2017
Summary
MicroRNA-146a (miR-146a) plays a key role in allergic conjunctivitis (AC). Decreased miR-146a in T cells exacerbates AC by affecting regulatory T cells (Tregs) and the NF-κB pathway.
Area of Science:
- Immunology
- Molecular Biology
Background:
- Allergic conjunctivitis (AC) is an inflammatory eye condition.
- The role of microRNAs in AC pathogenesis is an area of active research.
Purpose of the Study:
- To elucidate the regulatory mechanism of miR-146a in allergic conjunctivitis.
- To investigate the involvement of CD4+CD25- T cells in miR-146a's function.
Main Methods:
- Developed a mouse model of allergic conjunctivitis using ragweed pollen.
- Assessed eosinophil infiltration, IgE, and cytokine levels (IL-5, IL-13).
- Quantified miR-146a expression and analyzed T cell populations (Tregs, Tcons) via qRT-PCR and flow cytometry.
Main Results:
- miR-146a overexpression ameliorated AC symptoms in mice.
- miR-146a mimic transfection reduced splenocyte proliferation and IL-5/IL-13 expression.
- Decreased miR-146a in Tcons correlated with impaired Treg inhibition and NF-κB pathway activation, increasing IL-5/IL-13.
Conclusions:
- Reduced miR-146a in Tcons contributes to AC development.
- This occurs via modulation of Treg inhibitory function and the NF-κB signaling pathway.
