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• W3162458746 abstract "Abstract IL-4 production is associated with low-avidity, poorly cytotoxic T cell induction that contributes to viral immune evasion and the failure of T cell-based vaccines. Yet, the precise mechanisms that regulate IL-4 signalling in T cells remain elusive. Mounting evidence indicates that cells can dynamically alter their IL-4/IL-13 receptor signature to modulate downstream immune outcomes upon pathogen encounter. Here, we describe how naïve (CD62L + CD44 lo–mid ) CD4 and CD8 T cells distinctly engage both STAT6 and STAT3 in response to IL-4. We further show that IL-4R⍺ expression is both time- and IL-4 concentration-dependent. Remarkably, our findings reveal that STAT3 inhibition can ablate IL-4R⍺ and affect transcriptional expression of other Stat and Jak family members. By extension, the loss of STAT3 lead to aberrant STAT6 phosphorylation, revealing an inter-regulatory relationship between the two transcription factors. Moreover, IL-4 stimulation down-regulated TGF-β1 and IFN-γR1 expression on naïve T cells, possibly signifying the broad regulatory implications of IL-4 in conditioning lineage commitment decisions during early infection. Surprisingly, naïve T cells were unresponsive to IL-13 stimulation, unlike dendritic cells. Collectively, these findings could be exploited to inform more efficacious vaccines, as well as design treatments against IL-4/IL-13-associated disease conditions." @default.
• W3162458746 created "2021-05-24" @default.
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• W3162458746 date "2021-05-18" @default.
• W3162458746 modified "2023-10-11" @default.
• W3162458746 title "STAT3 determines IL-4 signalling outcomes in naïve T cells" @default.
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• W3162458746 doi "https://doi.org/10.1038/s41598-021-89860-7" @default.
• W3162458746 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8131749" @default.
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