E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung
Abstract Allergic airway inflammation is a universal airway disease induced by inhaling allergens. Published data show that RNF128, an E3 ligase, promotes Th2 activation in the OVA-induced asthma model. Recent advances have shown that group 2 innate lymphoid cells (ILC2s) produce the cytokines IL-5...
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Nature Portfolio
2025-01-01
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| Online Access: | https://doi.org/10.1038/s41598-025-85227-4 |
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| author | Chenghua Yan Wendong Kuang Guangqiang Ma Feifei Guo Liang Jin Hongjiao Wan Jinhua Zhu Yongcui Liao Haijun Tan Liyuan Wang |
| author_facet | Chenghua Yan Wendong Kuang Guangqiang Ma Feifei Guo Liang Jin Hongjiao Wan Jinhua Zhu Yongcui Liao Haijun Tan Liyuan Wang |
| author_sort | Chenghua Yan |
| collection | DOAJ |
| description | Abstract Allergic airway inflammation is a universal airway disease induced by inhaling allergens. Published data show that RNF128, an E3 ligase, promotes Th2 activation in the OVA-induced asthma model. Recent advances have shown that group 2 innate lymphoid cells (ILC2s) produce the cytokines IL-5 and IL-13 to mediate type 2 immune response. However, whether RNF128 regulates ILC2-dependent allergic lung inflammation remains unclear. In this study, we observed greater expression of the E3 ligase RNF128 in ILC2s than in other immune cells. RNF128 deficiency caused a selective increase in the number of peripheral mature ILC2s, and mice with RNF128 deficiency were more susceptible to Alternaria alternata (A. alternata) -induced allergic lung inflammation. Furthermore, RNF128 deficiency increased recruitment of eosinophils and levels of IL-5 and IL-13 in the bronchoalveolar lavage fluid. RNF128 effectively inhibited the expansion of ILC2s and the number of IL-5- and IL-13-producing ILC2s. Specially, RNF128 deficiency promoted the expression of the interleukin-33 (IL-33) receptor ST2 in A. alternata-induced allergic lung inflammation. Above all, our study demonstrated that RNF128 played a key role in A. alternata-induced ILC2 activation and type 2 immune response, suggesting that RNF128 may be an effective therapeutic target for allergic lung inflammation initiated by ILC2s. |
| format | Article |
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| institution | Kabale University |
| issn | 2045-2322 |
| language | English |
| publishDate | 2025-01-01 |
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| spelling | doaj-art-676da8914057439ea662f9a44eb3ceec2025-01-12T12:16:42ZengNature PortfolioScientific Reports2045-23222025-01-011511810.1038/s41598-025-85227-4E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lungChenghua Yan0Wendong Kuang1Guangqiang Ma2Feifei Guo3Liang Jin4Hongjiao Wan5Jinhua Zhu6Yongcui Liao7Haijun Tan8Liyuan Wang9College of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese MedicineInstitute of Microbiology, Jiangxi Academy of SciencesCollege of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese MedicineCollege of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese MedicineInstitute of Biological Resources, Jiangxi Academy of SciencesCollege of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese MedicineCollege of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese MedicineCollege of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese MedicineChina Animal Husbandry Industry Co., LtdCollege of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese MedicineAbstract Allergic airway inflammation is a universal airway disease induced by inhaling allergens. Published data show that RNF128, an E3 ligase, promotes Th2 activation in the OVA-induced asthma model. Recent advances have shown that group 2 innate lymphoid cells (ILC2s) produce the cytokines IL-5 and IL-13 to mediate type 2 immune response. However, whether RNF128 regulates ILC2-dependent allergic lung inflammation remains unclear. In this study, we observed greater expression of the E3 ligase RNF128 in ILC2s than in other immune cells. RNF128 deficiency caused a selective increase in the number of peripheral mature ILC2s, and mice with RNF128 deficiency were more susceptible to Alternaria alternata (A. alternata) -induced allergic lung inflammation. Furthermore, RNF128 deficiency increased recruitment of eosinophils and levels of IL-5 and IL-13 in the bronchoalveolar lavage fluid. RNF128 effectively inhibited the expansion of ILC2s and the number of IL-5- and IL-13-producing ILC2s. Specially, RNF128 deficiency promoted the expression of the interleukin-33 (IL-33) receptor ST2 in A. alternata-induced allergic lung inflammation. Above all, our study demonstrated that RNF128 played a key role in A. alternata-induced ILC2 activation and type 2 immune response, suggesting that RNF128 may be an effective therapeutic target for allergic lung inflammation initiated by ILC2s.https://doi.org/10.1038/s41598-025-85227-4E3 ligase RNF128Group 2 innate lymphoid cellsAllergic lung inflammation |
| spellingShingle | Chenghua Yan Wendong Kuang Guangqiang Ma Feifei Guo Liang Jin Hongjiao Wan Jinhua Zhu Yongcui Liao Haijun Tan Liyuan Wang E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung Scientific Reports E3 ligase RNF128 Group 2 innate lymphoid cells Allergic lung inflammation |
| title | E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung |
| title_full | E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung |
| title_fullStr | E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung |
| title_full_unstemmed | E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung |
| title_short | E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung |
| title_sort | e3 ligase rnf128 restricts a alternata induced ilc2 activation and type 2 immune response in the murine lung |
| topic | E3 ligase RNF128 Group 2 innate lymphoid cells Allergic lung inflammation |
| url | https://doi.org/10.1038/s41598-025-85227-4 |
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