Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8
BackgroundThe airway epithelial barrier is the first defence against aeroallergens. Nasal epithelial cells (NECs) are vital in regulating innate and adaptive mucosal immunity in allergic rhinitis (AR). Tregs produce cytokines essential for the immunomodulatory activities in allergen immunotherapy. U...
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Frontiers Media S.A.
2025-02-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1526081/full |
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| author | Jichao Sha Maolin Yang Yashu Lei Liwei Sun Cuida Meng Dongdong Zhu |
| author_facet | Jichao Sha Maolin Yang Yashu Lei Liwei Sun Cuida Meng Dongdong Zhu |
| author_sort | Jichao Sha |
| collection | DOAJ |
| description | BackgroundThe airway epithelial barrier is the first defence against aeroallergens. Nasal epithelial cells (NECs) are vital in regulating innate and adaptive mucosal immunity in allergic rhinitis (AR). Tregs produce cytokines essential for the immunomodulatory activities in allergen immunotherapy. Understanding the relationship between NECs and Tregs in the airway hyperresponsiveness network is essential for developing novel treatments.MethodsUsing an in vitro human Treg-NEC co-culture system of AR and health control group, the chemokine expression profiles of NECs were examined using immunohistochemistry, RT-PCR, and ELISA, and functional surface markers of Tregs were detected using flow cytometric analysis. Correlation analysis was performed between cytokines derived from NECs and surface markers of CD4+CD8+Foxp3+ Tregs in the AR group after co-culture, including TSLP/CTLA4, CCL1/CTLA4, TSLP/CTLA4, TSLP/CCR8, and CCL1/CCR8.ResultsCCR8 and CTLA-4 expressions after co-culturing were higher than single culture. Following Derp1 stimulation, TSLP, IL-25 and TGF-β expressions in the AR + Derp1 group were increased. CCL1 mRNA was lower in the AR + Derp1 group than control group. In the AR + Derp1 group, TSLP was higher, and CCL1 protein levels were decreased. There were no significant differences in IL-25, TGF-β and IL-10. When Treg co-culture group added, changes were similar to that observed in pNECs. After co-culture, CCL1/CCR8 was positively correlated in AR.ConclusionHuman pNECs can communicate with Tregs directly, CCL1/CCR8 may be the pathway between NECs and Tregs in vitro and may play a key role in the immune network of AR. |
| format | Article |
| id | doaj-art-84afd2b043f3472fa7fd59d166eda5fd |
| institution | DOAJ |
| issn | 1664-3224 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj-art-84afd2b043f3472fa7fd59d166eda5fd2025-08-20T03:00:55ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-02-011610.3389/fimmu.2025.15260811526081Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8Jichao ShaMaolin YangYashu LeiLiwei SunCuida MengDongdong ZhuBackgroundThe airway epithelial barrier is the first defence against aeroallergens. Nasal epithelial cells (NECs) are vital in regulating innate and adaptive mucosal immunity in allergic rhinitis (AR). Tregs produce cytokines essential for the immunomodulatory activities in allergen immunotherapy. Understanding the relationship between NECs and Tregs in the airway hyperresponsiveness network is essential for developing novel treatments.MethodsUsing an in vitro human Treg-NEC co-culture system of AR and health control group, the chemokine expression profiles of NECs were examined using immunohistochemistry, RT-PCR, and ELISA, and functional surface markers of Tregs were detected using flow cytometric analysis. Correlation analysis was performed between cytokines derived from NECs and surface markers of CD4+CD8+Foxp3+ Tregs in the AR group after co-culture, including TSLP/CTLA4, CCL1/CTLA4, TSLP/CTLA4, TSLP/CCR8, and CCL1/CCR8.ResultsCCR8 and CTLA-4 expressions after co-culturing were higher than single culture. Following Derp1 stimulation, TSLP, IL-25 and TGF-β expressions in the AR + Derp1 group were increased. CCL1 mRNA was lower in the AR + Derp1 group than control group. In the AR + Derp1 group, TSLP was higher, and CCL1 protein levels were decreased. There were no significant differences in IL-25, TGF-β and IL-10. When Treg co-culture group added, changes were similar to that observed in pNECs. After co-culture, CCL1/CCR8 was positively correlated in AR.ConclusionHuman pNECs can communicate with Tregs directly, CCL1/CCR8 may be the pathway between NECs and Tregs in vitro and may play a key role in the immune network of AR.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1526081/fullallergic rhinitisnasal epithelial cellsregulatory T cellscytokinesCC chemokine ligand 1 |
| spellingShingle | Jichao Sha Maolin Yang Yashu Lei Liwei Sun Cuida Meng Dongdong Zhu Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8 Frontiers in Immunology allergic rhinitis nasal epithelial cells regulatory T cells cytokines CC chemokine ligand 1 |
| title | Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8 |
| title_full | Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8 |
| title_fullStr | Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8 |
| title_full_unstemmed | Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8 |
| title_short | Interaction between nasal epithelial cells and Tregs in allergic rhinitis responses to allergen via CCL1/CCR8 |
| title_sort | interaction between nasal epithelial cells and tregs in allergic rhinitis responses to allergen via ccl1 ccr8 |
| topic | allergic rhinitis nasal epithelial cells regulatory T cells cytokines CC chemokine ligand 1 |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1526081/full |
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