ArticleMucosal immunology2025
T-cell immunity against influenza virus does not require Th1 or Th17 master regulator transcription factors.
Article in Mucosal immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- T-cell-mediated immunity to influenza A (H2N3): implications for caccine efficacy and cross-subtype protection.Archives of microbiology · 2026Review
- Machine learning for early screening of influenza A-associated invasive pulmonary aspergillosis in hospitalized patients: a real-world study.Frontiers in cellular and infection microbiology · 2026Article
- Effects of occupational stress on the distribution of circulating T lymphocyte subsets and psychological health of young anaesthesiologists.BMC psychology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Transcriptional programming needed for CD4 T cell immunity against influenza A virus (IAV) is unclear. Most antiviral CD4 T cells fit Th1 criteria, but cells unable to develop Th1 identity, through deletion of the transcription factors T-bet and Eomesodermin, remain protective. These double knockout (DKO) cells produce Th17 cytokines and express the Th17 'master regulator', Rorγt, supporting the concept that Th17 programming is needed for Th1-independent T cell immunity. Here, we directly tested requirements for Rorγt in promoting this mode of protection using T-bet/Eomesodermin/Rorγt triple knockout (TKO) mice. We show that Th17 functions are dramatically reduced in TKO cells but that they can nevertheless transfer protection against IAV to unprimed wildtype mice. Furthermore, TKO mice efficiently clear primary IAV infection, resist lethal bacterial superinfection, and generate antibody-dependent immunity against reinfection with the same virus. Finally, T cell-dependent heterosubtypic immunity is similarly effective in IAV-primed TKO, DKO, and wildtype mice. However, strikingly different T cell response patterns and inflammatory landscapes underlie these protective outcomes, highlighted in TKO mice by Th2-linked components not typically associated with efficient viral clearance. Our results reveal an unexpected degree of flexibility in T cell responses able to combat IAV, underscoring their potential to enhance vaccine strategies.
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Registered trials
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