ArticleThe journal of allergy and clinical immunology. Global2024
Apolipoprotein A-I inhibited group II innate lymphoid cell response mediated by microRNA-155 in allergic rhinitis.
Article in The journal of allergy and clinical immunology. Global, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 2 citations in OpenAlex.
- MicroRNA‑microbiome cross‑kingdom networks drive inflammatory bowel disease through dynamic regulatory ecosystems (Review).International journal of molecular medicine · 2026Review
- Routine lipid profiles in allergic disease: a mini review.Frontiers in allergy · 2026Review
- Apolipoprotein E promoted the proliferation and function of group 2 innate lymphoid cells through low density lipoprotein receptor in allergic rhinitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Interleukin-37 Suppresses the Function of Type 2 Follicular Helper T in Allergic Rhinitis.Biomedicines · 2025Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Group 2 innate lymphoid cells (ILC2s) have been found to take part in type 2 inflammation by secreting T Objective: We aimed to investigate the effect of Apo-AI on the proliferation and function of ILC2s as well as its possible mechanism. Methods: The protein expression of Apo-AI and the percentage of ILC2s in peripheral blood between 20 allergic rhinitis patients and 20 controls were detected by ELISA and flow cytometry. The effect of Apo-AI and miR-155 on ILC2 proliferation and function was detected by tritiated thymidine incorporation and ELISA. Anima models were adopted to verify the effect of Apo-AI Results: Elevated expression of Apo-AI was observed in allergic rhinitis patients. Apo-AI promotes Conclusion: Apo-AI suppressed the proliferation and function of ILC2s through miR-155 in allergic rhinitis. Our data provide new insights into the mechanism of allergen-induced airway inflammation.
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Registered trials
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