Abstract
We demonstrate that the mechanism of redox remodeling during mouse T cell activation involves secretion of glutathione by dendritic cells and its subsequent cleavage to cysteine. Extracellular cysteine accumulation results in a lower redox potential, which is conducive to proliferation, and changes the net redox status of exofacial protein domains. Regulatory T cells inhibit this redox metabolite-signaling pathway, which represents a previously unrecognized mechanism for immunosuppression of effector T cells.
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