MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus
Abstract Introduction Further investigation is required to determine the etiology of systemic lupus erythematosus (SLE). The aim of this study is to assess the presence of miR-223 within neutrophils in SLE and investigate its impact on the expansion of Th17 cells. Methods Experiments were performed...
Saved in:
| Main Authors: | , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
BMC
2025-02-01
|
| Series: | Arthritis Research & Therapy |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s13075-025-03487-x |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1823861724003958784 |
|---|---|
| author | Chengzhong Zhang Yan Lu |
| author_facet | Chengzhong Zhang Yan Lu |
| author_sort | Chengzhong Zhang |
| collection | DOAJ |
| description | Abstract Introduction Further investigation is required to determine the etiology of systemic lupus erythematosus (SLE). The aim of this study is to assess the presence of miR-223 within neutrophils in SLE and investigate its impact on the expansion of Th17 cells. Methods Experiments were performed in MRL/lpr mice, which were divided into control and miR-223 knockdown (miR-223-) group. We assessed miR-223 expression within neutrophils and Th17 expansion in MRL/lpr mice and patients with SLE using RT-PCR, luciferase reporter assay, Elisa, flow cytometry analysis. Signaling pathway, RT-PCR and western blot were conducted to elucidate the mechanism by which miR-223 within neutrophils expands Th17. Results We initially identified miR-223 as a pivotal factor in the pathogenesis of SLE in both MRL/lpr mice and SLE patients. Subsequently, knockdown of miR-223 led to a significant reduction in Th17 expansion in MRL/lpr mice. Moreover, inhibition of miR-223 effectively attenuated the recruitment and activation of neutrophils in SLE. Furthermore, we found rb6-8c5 treatment alleviated lupus symptoms of MRL/lpr mice and reduce the level of Th17. Finally, we elucidated that neutrophils potentiate the induction of Th17 through the activation of thePI3K-AKT pathway mediated by miR-223 during SLE-associated Th17 expansion. Conclusion MiR-223 within neutrophil axis contributes to Th17 expansion by PI3K-AKT pathway in SLE, and miR-223 could be a therapeutic target of SLE. |
| format | Article |
| id | doaj-art-64a9723b44d94120b9eacc59aa1e686e |
| institution | Kabale University |
| issn | 1478-6362 |
| language | English |
| publishDate | 2025-02-01 |
| publisher | BMC |
| record_format | Article |
| series | Arthritis Research & Therapy |
| spelling | doaj-art-64a9723b44d94120b9eacc59aa1e686e2025-02-09T12:48:45ZengBMCArthritis Research & Therapy1478-63622025-02-0127111310.1186/s13075-025-03487-xMiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosusChengzhong Zhang0Yan Lu1Department of Dermatology, the First affiliated Hospital of Nanjing Medical UniversityDepartment of Dermatology, the First affiliated Hospital of Nanjing Medical UniversityAbstract Introduction Further investigation is required to determine the etiology of systemic lupus erythematosus (SLE). The aim of this study is to assess the presence of miR-223 within neutrophils in SLE and investigate its impact on the expansion of Th17 cells. Methods Experiments were performed in MRL/lpr mice, which were divided into control and miR-223 knockdown (miR-223-) group. We assessed miR-223 expression within neutrophils and Th17 expansion in MRL/lpr mice and patients with SLE using RT-PCR, luciferase reporter assay, Elisa, flow cytometry analysis. Signaling pathway, RT-PCR and western blot were conducted to elucidate the mechanism by which miR-223 within neutrophils expands Th17. Results We initially identified miR-223 as a pivotal factor in the pathogenesis of SLE in both MRL/lpr mice and SLE patients. Subsequently, knockdown of miR-223 led to a significant reduction in Th17 expansion in MRL/lpr mice. Moreover, inhibition of miR-223 effectively attenuated the recruitment and activation of neutrophils in SLE. Furthermore, we found rb6-8c5 treatment alleviated lupus symptoms of MRL/lpr mice and reduce the level of Th17. Finally, we elucidated that neutrophils potentiate the induction of Th17 through the activation of thePI3K-AKT pathway mediated by miR-223 during SLE-associated Th17 expansion. Conclusion MiR-223 within neutrophil axis contributes to Th17 expansion by PI3K-AKT pathway in SLE, and miR-223 could be a therapeutic target of SLE.https://doi.org/10.1186/s13075-025-03487-xSystemic lupus erythematousmiR-223NeutrophilTh17 |
| spellingShingle | Chengzhong Zhang Yan Lu MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus Arthritis Research & Therapy Systemic lupus erythematous miR-223 Neutrophil Th17 |
| title | MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus |
| title_full | MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus |
| title_fullStr | MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus |
| title_full_unstemmed | MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus |
| title_short | MiR-223 within neutrophil axis promotes Th17 expansion by PI3K-AKT pathway in systemic lupus erythematosus |
| title_sort | mir 223 within neutrophil axis promotes th17 expansion by pi3k akt pathway in systemic lupus erythematosus |
| topic | Systemic lupus erythematous miR-223 Neutrophil Th17 |
| url | https://doi.org/10.1186/s13075-025-03487-x |
| work_keys_str_mv | AT chengzhongzhang mir223withinneutrophilaxispromotesth17expansionbypi3kaktpathwayinsystemiclupuserythematosus AT yanlu mir223withinneutrophilaxispromotesth17expansionbypi3kaktpathwayinsystemiclupuserythematosus |