Cellular signalling · 2026
Notch2-expressing regulatory T cells attenuate allergic rhinitis by downregulating MHC class II expression on dendritic cells.
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Zhou Yan-Ting, Xi Yang, Zhong Dian, Xu Shan, Yang Rui, Qiao Yue-Long, Kong Yong-Gang, Jiao Wo-Er, Chen Shi-Ming
Аннотация
AIMS: To investigate the role of Notch2-expressing regulatory T cells (Notch2+ Tregs) in modulating the function of dendritic cells (DCs) and their impact on the development of allergic rhinitis (AR).
METHODS: Peripheral blood mononuclear cells (PBMC) from patients with allergic rhinitis (AR) and Control groups were analyzed by flow cytometry to quantify Notch2+ Tregs. Murine T cells were isolated and transduced with a lentiviral vector overexpressing Notch2 to assess changes in the immunosuppressive function of Tregs. Scanning electron microscopy (SEM) was performed to visualize the morphological interactions between Tregs and Bone marrow-derived dendritic cells (BMDCs). BMDCs were cocultured with Notch2-overexpressing or control Tregs in direct-contact and Transwell coculture systems to evaluate changes in surface MHC class II (MHC II) expression. In vivo, Notch2-overexpressing Tregs were adoptively transferred into a conventional AR mouse model, after which the Treg and DC frequencies, surface MHC II expression, and allergic inflammatory responses were assessed.
RESULTS: Patients with AR had a significantly lower frequency of peripheral Notch2+ Tregs than controls (P < 0.01), and Notch2+ Treg frequency was negatively correlated with allergen-specific IgE levels and TNSS (P < 0.01). In vitro, Notch2 enhanced the immunosuppressive function of Tregs, increased MHC II expression on Tregs, and decreased MHC II expression on DCs. In vivo, adoptive transfer of Notch2-overexpressing Tregs significantly alleviated allergic inflammation in AR mice by reducing MHC II expression on DCs (P < 0.05).
CONCLUSION: Notch2 attenuates allergic inflammation in AR by enhancing Treg immunosuppressive function and downregulating MHC II expression on DCs. Notch2 in Tregs may represent a novel therapeutic target for allergic airway diseases.
METHODS: Peripheral blood mononuclear cells (PBMC) from patients with allergic rhinitis (AR) and Control groups were analyzed by flow cytometry to quantify Notch2+ Tregs. Murine T cells were isolated and transduced with a lentiviral vector overexpressing Notch2 to assess changes in the immunosuppressive function of Tregs. Scanning electron microscopy (SEM) was performed to visualize the morphological interactions between Tregs and Bone marrow-derived dendritic cells (BMDCs). BMDCs were cocultured with Notch2-overexpressing or control Tregs in direct-contact and Transwell coculture systems to evaluate changes in surface MHC class II (MHC II) expression. In vivo, Notch2-overexpressing Tregs were adoptively transferred into a conventional AR mouse model, after which the Treg and DC frequencies, surface MHC II expression, and allergic inflammatory responses were assessed.
RESULTS: Patients with AR had a significantly lower frequency of peripheral Notch2+ Tregs than controls (P < 0.01), and Notch2+ Treg frequency was negatively correlated with allergen-specific IgE levels and TNSS (P < 0.01). In vitro, Notch2 enhanced the immunosuppressive function of Tregs, increased MHC II expression on Tregs, and decreased MHC II expression on DCs. In vivo, adoptive transfer of Notch2-overexpressing Tregs significantly alleviated allergic inflammation in AR mice by reducing MHC II expression on DCs (P < 0.05).
CONCLUSION: Notch2 attenuates allergic inflammation in AR by enhancing Treg immunosuppressive function and downregulating MHC II expression on DCs. Notch2 in Tregs may represent a novel therapeutic target for allergic airway diseases.