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已发表论文
单细胞多组学揭示脓毒症相关 T 细胞功能障碍的核心基因网络及免疫相互作用崩溃
Authors Li X , Chen Z, Yao Y, Chen M, Hu Y
Received 7 May 2025
Accepted for publication 7 September 2025
Published 13 September 2025 Volume 2025:18 Pages 4863—4885
DOI https://doi.org/10.2147/IDR.S538883
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Yan Li
Xiang Li, Zhibin Chen, Yandong Yao, Muhu Chen, Yingchun Hu
Department of Emergency Medicine, The Affiliated Hospital, Southwest Medical University, Luzhou, 646000, People’s Republic of China
Correspondence: Muhu Chen; Yingchun Hu, Email cmh6186@swmu.edu.cn; huyingchun913@swmu.edu.cn
Introduction: Sepsis is a life-threatening condition characterized by immune dysregulation, yet the mechanisms underlying T cell dysfunction remain poorly understood.
Methods: We integrated multi-omics data from public GEO datasets and prospective cohorts. Single-cell transcriptomic analysis was applied to identify core genes, followed by diagnostic and prognostic validation. Cell–cell interaction networks were constructed to investigate signaling alterations, and cross-platform validation was conducted.
Results: Seven core genes (LTB, CD3D, TRAF3IP3, CD3G, GZMM, HLA-DPB1, CD3E) were identified, showing strong diagnostic value (AUC ≥ 0.86) and prognostic significance (HR=4.50 for CD3E). Network analysis revealed collapse of critical signaling axes (HLA-DRA-MHCII, ITGB2-CD226) and aberrant activation of inhibitory pathways (LGALS9-CD45), leading to a “co-stimulation inhibition–checkpoint activation” imbalance. Cross-platform validation confirmed conserved downregulation of these genes in sepsis, which contributed to immune exhaustion via disrupted T cell differentiation trajectories and impaired intercellular communication.
Conclusion: Our findings highlight novel biomarkers and potential therapeutic targets for sepsis immunotherapy by systematically deciphering core gene networks and immune interaction collapse in T cell dysfunction.
Keywords: sepsis, single-cell rna sequencing, t cell exhaustion, biomarkers, cell-cell communication
Department of Emergency Medicine, The Affiliated Hospital, Southwest Medical University, Luzhou, 646000, People’s Republic of China
Correspondence: Muhu Chen; Yingchun Hu, Email cmh6186@swmu.edu.cn; huyingchun913@swmu.edu.cn
Introduction: Sepsis is a life-threatening condition characterized by immune dysregulation, yet the mechanisms underlying T cell dysfunction remain poorly understood.
Methods: We integrated multi-omics data from public GEO datasets and prospective cohorts. Single-cell transcriptomic analysis was applied to identify core genes, followed by diagnostic and prognostic validation. Cell–cell interaction networks were constructed to investigate signaling alterations, and cross-platform validation was conducted.
Results: Seven core genes (LTB, CD3D, TRAF3IP3, CD3G, GZMM, HLA-DPB1, CD3E) were identified, showing strong diagnostic value (AUC ≥ 0.86) and prognostic significance (HR=4.50 for CD3E). Network analysis revealed collapse of critical signaling axes (HLA-DRA-MHCII, ITGB2-CD226) and aberrant activation of inhibitory pathways (LGALS9-CD45), leading to a “co-stimulation inhibition–checkpoint activation” imbalance. Cross-platform validation confirmed conserved downregulation of these genes in sepsis, which contributed to immune exhaustion via disrupted T cell differentiation trajectories and impaired intercellular communication.
Conclusion: Our findings highlight novel biomarkers and potential therapeutic targets for sepsis immunotherapy by systematically deciphering core gene networks and immune interaction collapse in T cell dysfunction.
Keywords: sepsis, single-cell rna sequencing, t cell exhaustion, biomarkers, cell-cell communication