TNF and bacterial infectious disease: A previous study showed that NEMO dimerization via disulfide bonds and subsequent NF-κB signaling after TNF stimulation in mouse embryonic fibroblasts (MEF) depended on two redox-sensitive cysteines, Cys54 and Cys374, [40] and, indeed, expression of a redox-insensitive NEMO mutant in PM, BMDM and MEF through transfection of in vitro-generated mRNA [123] completely abolished disulfide linkage of NEMO, proinflammatory signaling and cytokine secretion in response to bacterial infection.