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已发表论文
系统性红斑狼疮中血浆外泌体 LncRNA XIST 通过 miR-98/RICTOR/Akt-mTOR 轴损害 CD4+ T 细胞自噬并促进其活化
Authors Wang L, Lyu F, Liang J, Chen X, Zheng C, Chu M, Xu J, Xie L
Received 20 October 2025
Accepted for publication 19 January 2026
Published 12 February 2026 Volume 2026:19 574715
DOI https://doi.org/10.2147/JIR.S574715
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Adrian Lee
Li Wang,1,* Fan Lyu,1,* Jun Liang,1 Xi Chen,1 Chenghui Zheng,1 Mingyu Chu,1 Jinhua Xu,1,2 Lin Xie1
1Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China; 2Shanghai Institute of Dermatology, Shanghai, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Lin Xie, Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, People’s Republic of China, Email xielin@fudan.edu.cn Jinhua Xu, Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, People’s Republic of China, Email jinhuaxu@fudan.edu.cn
Background: Systemic lupus erythematosus (SLE) is characterized by immune dysregulation driven in part by aberrant CD4+ T cell activation and defective autophagy. Although exosomes are increasingly recognized as mediators of immune communication, the contribution of exosomal long non-coding RNAs (lncRNAs) to T cell dysfunction in SLE remains poorly defined. This study investigated the pathogenic role and mechanism of plasma exosomal lncRNA XIST in regulating CD4+ T cell autophagy and activation.
Methods: Quantitative reverse transcription PCR (qRT-PCR) was used to quantify lncRNA XIST levels in plasma exosomes, while Western blotting, flow cytometry, and enzyme-linked immunosorbent assay (ELISA) were employed to assess the effects of exosomes on CD4+ T cell function. Gain- and loss-of-function approaches were applied to elucidate the underlying molecular mechanisms.
Results: LncRNA XIST was significantly overexpressed in SLE plasma exosomes and positively correlated with disease activity. These exosomes enhanced lncRNA XIST expression in CD4+ T cells from healthy controls (HCs), leading to suppressed autophagy and increased activation. Similar effects were observed with engineered HC plasma exosomes overexpressing lncRNA XIST. Conversely, silencing lncRNA XIST in SLE CD4+ T cells promoted autophagy and reduced activation, although these changes were reversed upon treatment with autologous plasma exosomes. Mechanistically, exosomal XIST functioned as a molecular sponge for miR-98, upregulating RICTOR and activating the Akt/mTOR signaling pathway, thereby modulating CD4+ T cell function.
Conclusion: Plasma exosomal lncRNA XIST impairs CD4+ T cell autophagy and promotes activation through the miR-98/RICTOR/Akt-mTOR axis, representing a mechanistically defined candidate biomarker and potential therapeutic target in SLE.
Keywords: systemic lupus erythematosus, exosome, lncRNA XIST, CD4+ T cells, autophagy
1Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China; 2Shanghai Institute of Dermatology, Shanghai, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Lin Xie, Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, People’s Republic of China, Email xielin@fudan.edu.cn Jinhua Xu, Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, 200040, People’s Republic of China, Email jinhuaxu@fudan.edu.cn
Background: Systemic lupus erythematosus (SLE) is characterized by immune dysregulation driven in part by aberrant CD4+ T cell activation and defective autophagy. Although exosomes are increasingly recognized as mediators of immune communication, the contribution of exosomal long non-coding RNAs (lncRNAs) to T cell dysfunction in SLE remains poorly defined. This study investigated the pathogenic role and mechanism of plasma exosomal lncRNA XIST in regulating CD4+ T cell autophagy and activation.
Methods: Quantitative reverse transcription PCR (qRT-PCR) was used to quantify lncRNA XIST levels in plasma exosomes, while Western blotting, flow cytometry, and enzyme-linked immunosorbent assay (ELISA) were employed to assess the effects of exosomes on CD4+ T cell function. Gain- and loss-of-function approaches were applied to elucidate the underlying molecular mechanisms.
Results: LncRNA XIST was significantly overexpressed in SLE plasma exosomes and positively correlated with disease activity. These exosomes enhanced lncRNA XIST expression in CD4+ T cells from healthy controls (HCs), leading to suppressed autophagy and increased activation. Similar effects were observed with engineered HC plasma exosomes overexpressing lncRNA XIST. Conversely, silencing lncRNA XIST in SLE CD4+ T cells promoted autophagy and reduced activation, although these changes were reversed upon treatment with autologous plasma exosomes. Mechanistically, exosomal XIST functioned as a molecular sponge for miR-98, upregulating RICTOR and activating the Akt/mTOR signaling pathway, thereby modulating CD4+ T cell function.
Conclusion: Plasma exosomal lncRNA XIST impairs CD4+ T cell autophagy and promotes activation through the miR-98/RICTOR/Akt-mTOR axis, representing a mechanistically defined candidate biomarker and potential therapeutic target in SLE.
Keywords: systemic lupus erythematosus, exosome, lncRNA XIST, CD4+ T cells, autophagy