ArticleJournal of immunology (Baltimore, Md. : 1950)2022
Bona Fide Th17 Cells without Th1 Functional Plasticity Protect against Influenza.
Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Cell-Intrinsic Type I Interferon Signaling as a Pleiotropic Orchestrator of CD4 T Cell Immunity.Biomolecules · 2026Review
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- T-cell immunity against influenza virus does not require Th1 or Th17 master regulator transcription factors.Mucosal immunology · 2025Article
- Diversifying T-cell responses: safeguarding against pandemic influenza with mosaic nucleoprotein.Journal of virology · 2025Article
- Preexisting vaccine-primed heterosubtypic T cell immunity protects the maternal-fetal unit from adverse influenza outcomes in mice.The Journal of clinical investigation · 2025Article
- Article
- Review
- Review
- CD8Nature communications · 2023Article
- STAT1 Controls the Functionality of Influenza-Primed CD4 T Cells but Therapeutic STAT4 Engagement Maximizes Their Antiviral Impact.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Regulation of CD4 T Cell Responses by the Transcription Factor Eomesodermin.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Optimal transcriptional programming needed for CD4 T cells to protect against influenza A virus (IAV) is unclear. Most IAV-primed CD4 T cells fit Th1 criteria. However, cells deficient for the Th1 "master regulator," T-bet, although marked by reduced Th1 identity, retain robust protective capacity. In this study, we show that T-bet's paralog, Eomesodermin (Eomes), is largely redundant in the presence of T-bet but is essential for the residual Th1 attributes of T-bet-deficient cells. Cells lacking both T-bet and Eomes instead develop concurrent Th17 and Th2 responses driven by specific inflammatory signals in the infected lung. Furthermore, the transfer of T-bet- and Eomes-deficient Th17, but not Th2, effector cells protects mice from lethal IAV infection. Importantly, these polyfunctional Th17 effectors do not display functional plasticity in vivo promoting gain of Th1 attributes seen in wild-type Th17 cells, which has clouded evaluation of the protective nature of Th17 programming in many studies. Finally, we show that primary and heterosubtypic IAV challenge is efficiently cleared in T-bet- and Eomes double-deficient mice without enhanced morbidity despite a strongly Th17-biased inflammatory response. Our studies thus demonstrate unexpectedly potent antiviral capacity of unadulterated Th17 responses against IAV, with important implications for vaccine design.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.