AI Article Synopsis
- - Long-COVID (LC) is defined by lingering symptoms for over 3 months post-COVID-19 infection, potentially caused by immune system dysregulation and chronic inflammation.
- - The study identifies specific CD4 T cell subpopulations in COVID-19 recovery and reveals that certain CCR6-expressing T cells are reduced in LC patients, while others increase.
- - LC patients demonstrate lower levels of IFN-γ-secreting CD8 T cells when exposed to the SARS-CoV-2 Spike protein, highlighting the importance of CCR6 in understanding LC's underlying mechanisms.
Article Abstract
Long-COVID (LC) is characterised by persistent symptoms for at least 3 months after acute infection. A dysregulation of the immune system and a persistent hyperinflammatory state may cause LC. LC patients present differences in activation and exhaustion states of innate and adaptive compartments. Different T CD4 cell subsets can be identified by differential expression of chemokine receptors (CCR). However, changes in T cells with expression of CCRs such as CCR6 and CXCR3 and their relationship with CD8 T cells remains unexplored in LC. Here, we performed unsupervised analysis and found CCR6 CD4 subpopulations enriched in COVID-19 convalescent individuals upon activation with SARS-CoV-2 peptides. SARS-CoV-2 specific CCR6 CD4 are decreased in LC patients, whereas CXCR3 CCR6 and CCR4 CCR6 CD4 T cells are increased. LC patients showed lower IFN-γ-secreting CD8 T cells after stimulation with SARS-CoV-2 Spike protein. This work underscores the role of CCR6 in the pathophysiology of LC.
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| http://dx.doi.org/10.1016/j.clim.2024.110267 | DOI Listing |
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