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- W4313360207 abstract "Abstract Nuclear factor erythroid 2-related factor 2 (Nrf2) is a stress activated transcription factor, activated by such stimuli as reactive oxygen and electrophilic stress. Upon activation Nrf2 accumulates in the nucleus and activates a battery of target genes, many of which are cytoprotective in function. We have previously shown that a common synthetic food additive, tBHQ, is a potent Nrf2 activator and suppresses certain events of human T cell activation, namely, IL-2 secretion, CD25 expression, and transactivation ability of NFkB. The purpose of our current studies was to develop a Nrf2-null human model, in which it can be determined whether the effects of tBHQ upon the early events of T cell activation are Nrf2-dependent. Treatment of both Wild-type and Nrf2-null Jurkat T cells revealed that the suppression of IL-2 and NFkB by tBHQ is largely Nrf2-independent, whereas the suppression of CD25 is partially dependent upon Nrf2. Although interesting, these studies left the question as to the role of Nrf2 in T cell activation largely unanswered. Therefore, we utilized a more potent and selective Nrf2 activator, CDDO-Im. CDDO-Im treatment resulted in a Nrf2-dependent suppression of IL-2 secretion and an inhibition of NFkB activity that was partially Nrf2-dependent. Taken together, our model is the first to show that activation of Nrf2 suppresses early events of human T cell activation (This work is funded by NIH grants ES018885, ES024966 and GM092715)." @default.
- W4313360207 created "2023-01-06" @default.
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- W4313360207 date "2017-05-01" @default.
- W4313360207 modified "2023-10-12" @default.
- W4313360207 title "The Nrf2 activators tBHQ and CDDO-Im have both Nrf2-dependent and – independent effects on human Jurkat T cell activation, as determined by CRISPR-Cas9 gene editing" @default.
- W4313360207 doi "https://doi.org/10.4049/jimmunol.198.supp.124.4" @default.
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