Disabling surveillance: bacterial type III secretion system effectors that suppress innate immunity

Abstract

Many Gram-negative bacterial pathogens of plants and animals are dependent on a type III protein secretion system (TTSS). TTSSs translocate effector proteins into host cells and are capable of modifying signal transduction pathways. The innate immune system of eukaryotes detects the presence of pathogens using specific pathogen recognition receptors (PRRs). Plant PRRs include the FLS2 receptor kinase and resistance proteins. Animal PRRs include Toll-like receptors and nucleotide-binding oligomerization domain proteins. PRRs initiate signal transduction pathways that include mitogen-activated protein kinase (MAPK) cascades that activate defence-related transcription factors. This results in induction of proinflammatory cytokines in animals, and hallmarks of defence in plants including the hypersensitive response, callose deposition and the production of pathogenesis-related proteins. Several type III effectors from animal and plant pathogens have evolved to counteract innate immunity. For example, the Yersinia YopJ/P cysteine protease and the Pseudomonas syringae HopPtoD2 protein tyrosine phosphatase inhibits defence-related MAPK kinase activity in animals and plants respectively. Thus, type III effectors can suppress signal transduction pathways activated by PRR surveillance systems. Understanding targets and activities of type III effectors will reveal much about bacterial pathogenicity and the innate immune system in plants and animals.