Significance: Production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) occur rapidly in response to attempted pathogen invasion of potential host plants. Such redox changes are sensed and transmitted to engage immune function, including the hypersensitive response, a programmed execution of challenged plant cells. Recent advances: Pathogen elicitors trigger changes in calcium that are sensed by calmodulin, calmodulin-like proteins and calcium-dependent protein kinases that activate ROS and RNS production. ROS and RNS production are compartmentalised within the cell and occur through multiple routes. MAPK cascades are engaged upstream and downstream of ROS and nitric oxide (NO) production. NO is increasingly recognised as a key signalling molecule, regulating downstream protein function through S-nitrosylation, the addition of an NO moiety to a reactive cysteine thiol. Critical issues: How multiple sources of ROS and RNS are coordinated is unclear. The putative protein sensors that detect and translate fluxes in ROS and RNS into differential gene expression are obscure. Protein tyrosine nitration following reaction of peroxynitrite with tyrosine residues has been proposed as another signalling mechanism or as a marker leading to protein degradation but the reversibility remains to be established. Future directions: Research is needed to identify the full spectrum of NO modified proteins with special emphasis on redox-activated transcription factors and their cognate target genes. A systems approach will be required to uncover the complexities integral to redox regulation of MAPK cascades, transcription factors and defence genes through the combined effects of calcium, phosphorylation, S-nitrosylation and protein tyrosine nitration.