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已发表论文
白细胞介素 - 27 与白细胞介素 - 2 协同调节冠状动脉疾病中 CD4⁺ T 细胞亚群及免疫失衡
Authors Cai Y , Tang H , Tang W, Tang W, Xu W, Wang Y, Ding Y, Yu J, Pan C, Li Z, Peng Y, Zhu R, Yu K, Zeng Q, Zhong Y
Received 8 June 2025
Accepted for publication 9 November 2025
Published 10 December 2025 Volume 2025:18 Pages 17253—17269
DOI https://doi.org/10.2147/JIR.S545568
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Dr Qing Lin
Yifan Cai,1– 3,* Hongxia Tang,4,* Wenwen Tang,5,* Wenjuan Tang,6 Wenbin Xu,1– 3 Yue Wang,1– 3 Yan Ding,1– 3 Jian Yu,1– 3 Chengliang Pan,1– 3 Zhiyang Li,1– 3 Yudong Peng,1– 3 Ruirui Zhu,1– 3 Kunwu Yu,1– 3 Qiutang Zeng,1– 3 Yucheng Zhong7
1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 2Hubei Key Laboratory of Biological Targeted Therapy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 3Hubei Provincial Engineering Research Center of Immunological Diagnosis and Therapy for Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 4Department of Rheumatology and Immunology, Wuhan Children’s Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, Hubei, People’s Republic of China; 5Cardiovascular Department, Wuhan No.9 Hospital, Wuhan, Hubei, People’s Republic of China; 6Radiology Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 7Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yucheng Zhong, Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, People’s Republic of China, Tel/Fax +86 158 7237 4991, Email zyc811029@126.com
Background: Coronary artery disease (CAD) is an immune-mediated disorder driven by dysregulated T cell responses. Interleukin-27 (IL-27) has immunoregulatory properties, but its role in CAD remains unclear. This study is the first to investigate the effects of IL-27 on CD4⁺LAP⁺ T cells in CAD and to explore its interaction with interleukin-2 (IL-2) in modulating immune imbalance.
Methods: CAD severity was quantified by the Gensini score. Plasma IL-27 and oxidized low-density lipoprotein (ox-LDL) were measured by ELISA. Flow cytometry assessed CD4⁺ T cell subsets, while qRT-PCR and Western blot evaluated lineage-specific transcription factors.
Results: IL-27 levels were elevated in acute coronary syndrome and correlated with ox-LDL and Gensini scores. Patients with severe CAD showed a Th1/Th17-dominant profile and reductions in Th2, CD4⁺LAP⁺, and Tregs. In vitro, IL-27 promoted Th1 differentiation via T-bet/IFN-γ upregulation and suppressed Th2, Th17, and regulatory subsets, counteracting IL-2–induced expansion of Tregs and CD4⁺LAP⁺ cells. These effects were dose dependent and favored pro-inflammatory responses.
Conclusion: IL-27 drives immune imbalance in CAD by reinforcing Th1 polarization and antagonizing IL-2–mediated regulation. Beyond mechanistic insights, these findings identify IL-27 as a potential biomarker for disease severity and a candidate therapeutic target in CAD.
Keywords: IL-27, coronary artery disease, Th1/Th2, Th17/CD4+LAP+ T cells
1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 2Hubei Key Laboratory of Biological Targeted Therapy, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 3Hubei Provincial Engineering Research Center of Immunological Diagnosis and Therapy for Cardiovascular Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 4Department of Rheumatology and Immunology, Wuhan Children’s Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, Hubei, People’s Republic of China; 5Cardiovascular Department, Wuhan No.9 Hospital, Wuhan, Hubei, People’s Republic of China; 6Radiology Department, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China; 7Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yucheng Zhong, Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Jianghan District, Wuhan, Hubei, 430022, People’s Republic of China, Tel/Fax +86 158 7237 4991, Email zyc811029@126.com
Background: Coronary artery disease (CAD) is an immune-mediated disorder driven by dysregulated T cell responses. Interleukin-27 (IL-27) has immunoregulatory properties, but its role in CAD remains unclear. This study is the first to investigate the effects of IL-27 on CD4⁺LAP⁺ T cells in CAD and to explore its interaction with interleukin-2 (IL-2) in modulating immune imbalance.
Methods: CAD severity was quantified by the Gensini score. Plasma IL-27 and oxidized low-density lipoprotein (ox-LDL) were measured by ELISA. Flow cytometry assessed CD4⁺ T cell subsets, while qRT-PCR and Western blot evaluated lineage-specific transcription factors.
Results: IL-27 levels were elevated in acute coronary syndrome and correlated with ox-LDL and Gensini scores. Patients with severe CAD showed a Th1/Th17-dominant profile and reductions in Th2, CD4⁺LAP⁺, and Tregs. In vitro, IL-27 promoted Th1 differentiation via T-bet/IFN-γ upregulation and suppressed Th2, Th17, and regulatory subsets, counteracting IL-2–induced expansion of Tregs and CD4⁺LAP⁺ cells. These effects were dose dependent and favored pro-inflammatory responses.
Conclusion: IL-27 drives immune imbalance in CAD by reinforcing Th1 polarization and antagonizing IL-2–mediated regulation. Beyond mechanistic insights, these findings identify IL-27 as a potential biomarker for disease severity and a candidate therapeutic target in CAD.
Keywords: IL-27, coronary artery disease, Th1/Th2, Th17/CD4+LAP+ T cells