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<p>Long COVID has emerged as a major global health concern, yet the long-term trajectory of immune recovery and its contribution to persistent symptoms remain to be elucidated. Here, we conducted a three-year longitudinal follow-up of the&#xa0;47 COVID-19 patients and applied single-cell RNA sequencing (scRNA-seq) and multiplex cytokine profiling to comprehensively characterize the peripheral immune landscape during convalescence. We observed persistent immune dysregulation up to three years post-infection, characterized by chronic inflammation and impaired restoration of naïve <i>CD4⁺</i> T cells, naïve <i>CD8⁺</i> T cells, and <i>SLC4A10⁺</i> MAIT cells—features reminiscent of immunosenescence. Notably, Th17 cells, rather than monocytes, emerged as key drivers of chronic inflammation beyond one year. We identified two distinct Th17 subsets: <i>RORC⁺</i> Th17 cells and <i>LTB⁺</i> Th17 cells. While <i>RORC⁺</i> Th17 cells were negatively correlated with inflammatory cytokine levels, <i>LTB⁺</i> Th17 cells showed proinflammatory features and were positively associated with long COVID symptoms. Sustained elevation of S100A8 and IL-16 in follow-up patients may contribute to the persistent presence of <i>LTB⁺</i> Th17 cells. Together, our study provides an in-depth longitudinal map of immune remodeling in COVID-19 convalescents, revealing key cellular and molecular drivers of sustained inflammation up to three years post-infection.</p>

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T cell-driven sustained inflammation and immune dysregulation mimicking immunosenescence for up to three years post-COVID-19

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月20日

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  • Tian Zheng,
  • Ru Gao,
  • Yiwei Liu,
  • Yeming Wang,
  • Chao Wu,
  • Li Guo,
  • Lan Chen,
  • Xinming Wang,
  • Yan Xiao,
  • Jingchuan Zhong,
  • Rongling Zhang,
  • Ying Wang,
  • Xianwen Ren,
  • Bin Cao,
  • Lili Ren,
  • Jianwei Wang

摘要

Long COVID has emerged as a major global health concern, yet the long-term trajectory of immune recovery and its contribution to persistent symptoms remain to be elucidated. Here, we conducted a three-year longitudinal follow-up of the 47 COVID-19 patients and applied single-cell RNA sequencing (scRNA-seq) and multiplex cytokine profiling to comprehensively characterize the peripheral immune landscape during convalescence. We observed persistent immune dysregulation up to three years post-infection, characterized by chronic inflammation and impaired restoration of naïve CD4⁺ T cells, naïve CD8⁺ T cells, and SLC4A10⁺ MAIT cells—features reminiscent of immunosenescence. Notably, Th17 cells, rather than monocytes, emerged as key drivers of chronic inflammation beyond one year. We identified two distinct Th17 subsets: RORC⁺ Th17 cells and LTB⁺ Th17 cells. While RORC⁺ Th17 cells were negatively correlated with inflammatory cytokine levels, LTB⁺ Th17 cells showed proinflammatory features and were positively associated with long COVID symptoms. Sustained elevation of S100A8 and IL-16 in follow-up patients may contribute to the persistent presence of LTB⁺ Th17 cells. Together, our study provides an in-depth longitudinal map of immune remodeling in COVID-19 convalescents, revealing key cellular and molecular drivers of sustained inflammation up to three years post-infection.