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In multiple sclerosis models, GLP-1 receptor activation reduces pathogenic Th1 and Th17 cell activity, inhibits microglial activation (the brain equivalent of macrophage inflammation), and may enhance remyelination processes

Our roGFP2 measurements confirm (i) that dynamic roGFP2 sensing (or the physiological glutathionylation/deglutathionylation of regular surface-exposed cysteinyl residues) requires a glutaredoxin activity, and (ii) that glutathionylated proteins or metabolites should be very transient redox species when GSH and glutaredoxins are present (unless they are stabilized by a kinetic uncoupling mechanism) 5,32,34,35,6164

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