Several inflammation-related processes, including inflammasome activation and interleukin (IL)-1β secretion, are dependent on redox signaling. However, the type of redox response involved as well as the relevant role of pro-oxidant and antioxidant events are matters of intense debate. By comparing leukemic myeloid cells, healthy monocytes and macrophages, as well as monocytes from patients carrying mutations in members of the Nod-like receptor (NLR) gene family, we have drawn a model that reconciles previous conflicting hypotheses. We propose that the redox state of resting inflammatory cells determines the type and extent of redox response to pattern recognition receptor stimulation, which in turn dictates the efficiency of inflammasome activation. The impact on genetic and acquired inflammatory diseases will be discussed.
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