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• W2968395147 endingPage "e1007989" @default.
• W2968395147 startingPage "e1007989" @default.
• W2968395147 abstract "Defining the most penetrating correlates of protective memory T cells is key for designing improved vaccines and T cell therapies. Here, we evaluate how interleukin (IL-2) production by memory CD4 T cells, a widely held indicator of their protective potential, impacts immune responses against murine influenza A virus (IAV). Unexpectedly, we show that IL-2-deficient memory CD4 T cells are more effective on a per cell basis at combating IAV than wild-type memory cells that produce IL-2. Improved outcomes orchestrated by IL-2-deficient cells include reduced weight loss and improved respiratory function that correlate with reduced levels of a broad array of inflammatory factors in the infected lung. Blocking CD70-CD27 signals to reduce CD4 T cell IL-2 production tempers the inflammation induced by wild-type memory CD4 T cells and improves the outcome of IAV infection in vaccinated mice. Finally, we show that IL-2 administration drives rapid and extremely potent lung inflammation involving NK cells, which can synergize with sublethal IAV infection to promote acute death. These results suggest that IL-2 production is not necessarily an indicator of protective CD4 T cells, and that the lung environment is particularly sensitive to IL-2-induced inflammation during viral infection." @default.
• W2968395147 created "2019-08-22" @default.
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• W2968395147 date "2019-08-14" @default.
• W2968395147 modified "2023-10-11" @default.
• W2968395147 title "Memory CD4 T cell-derived IL-2 synergizes with viral infection to exacerbate lung inflammation" @default.
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• W2968395147 doi "https://doi.org/10.1371/journal.ppat.1007989" @default.
• W2968395147 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6693742" @default.
• W2968395147 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31412088" @default.
• W2968395147 hasPublicationYear "2019" @default.
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