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TRPM2 Deficiency Attenuates Allergic Rhinitis-Like Inflammation With Altered Ca2+-NFAT Signaling, Treg Responses, and
Zhenke Huang1, Jianping Fan2, Xinxin Shan1
1Department of Otolaryngology, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai, China.
Immunity, Inflammation and Disease
|July 13, 2026
Summary
Transient Receptor Potential Melastatin 2 (TRPM2) plays a role in allergic rhinitis (AR) inflammation. TRPM2 knockout mice showed reduced AR symptoms and inflammation, suggesting TRPM2 as a potential therapeutic target for AR.
Area of Science:
- Immunology
- Molecular Biology
- Allergy Research
Background:
- Allergic rhinitis (AR) is a common condition impacting quality of life.
- Current AR treatments have limitations and potential side effects.
Purpose of the Study:
- Investigate the role of Transient Receptor Potential Melastatin 2 (TRPM2) in AR.
- Examine TRPM2's impact on T cell function, Th2 responses, and Ca2+-NFAT signaling.
Main Methods:
- Utilized TRPM2 knockout and wild-type mice in an ovalbumin-induced AR model.
- Employed behavioral, histopathological, immunological, qPCR, and Western blot analyses.
Main Results:
- TRPM2 knockout mice displayed decreased AR symptoms, inflammation, and IgE levels.
- TRPM2 deficiency reduced key inflammatory cytokines (IL-4, IL-5, IL-33) and Ca2+ influx.
- Reduced NFATc1 translocation and IL-2 production were observed in TRPM2 knockout mice.
Conclusions:
- TRPM2 contributes to AR-like inflammation via immune and Ca2+-NFAT pathways.
- TRPM2 inhibition may offer a therapeutic strategy for AR.
- Further research is needed to understand mechanistic and translational implications.
