Thioredoxin regulates T cell proliferation and aggravates the severity of influenza a virus infection
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Le résumé fourni par la source
Different functional T lymphocytes play important roles in the progression of IAV infection, including proliferation, recruitment, and effector activity. However, the immune changes of T cells during IAV infection are unclear, and the related targets are still to be explored. In this study, we used a multi-omics approach combining transcriptome and single-cell transcriptome analysis to identify TXN as a key target gene and elucidate its close association with T-cell proliferation. From these data, we identified 10 key differential genes through a combination of differential analysis, WGCNA, and Friends analysis and further identified that only TXN and S100A6 co-existed in the highly variable genes of proliferative T cells. Because TXN exhibits highly specific high expression in proliferative T cells, we focused on its related research and ultimately identified it as a target gene for IAV infection. Reports have suggested that simultaneous inhibition of the GSH and TXN pathways can effectively trigger cell death. This proves our hypothesis about a new direction of T cell death in IAV infection. Additionally, we found that T cell development after IAV infection was regulated and altered, but this study did not clearly explain whether it was negative regulation. In summary, we have identified TXN as a target gene involved in T cell proliferation during IAV infection, and we suggest that its expression may be associated with non-apoptotic forms of T cell death.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Thioredoxin regulates T cell proliferation and aggravates the severity of influenza a virus infection
- Date Crossref
- 08/07/2025
- Éditeur
- Springer Science and Business Media LLC
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
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