摘要：

Plants lack specialized mobile immune cells. Instead of this, each plant cell can recognize an attack of a pathogen and activate an effective immune response. Protection against pathogenic microorganisms is based on a plant's system of identifying danger signs. The danger signals may come from a pathogen or from a host plant itself. The innate immune system responds to infections at two layers. The first layer recognizes and responds to the molecular patterns shared by large groups of potential pathogens. Recognition is executed through pattern recognition receptors (PRRs) localized on the plasma membrane and followed by an immune response, the pattern-triggered immunity (PTI). The second layer responds to the virulence factors (effectors) of pathogenic microorganisms directly or through their impact on the host plant. The identification of a pathogen's effectors through intracellular receptors or those localized on the plasma membrane (ERRs) activates immune responses, the effector-triggered immunity (ETI). The article reviews the latest data on the mechanisms through which these receptors perceive patterns and effectors of pathogens and initiate immune responses. New ideas about the structure and function of plant immune receptors have led to changes in our understanding of PTI and ETI as well as of their interaction. Despite the variability in the intensity and duration of immune responses induced by different molecular patterns or pathogen effectors in PTI or ETI, the immune sensors are localized either in the plasma membrane or in cytoplasm and activate analogous molecular events, such as activation of MAP kinases, synthesis of reactive oxygen species, and calcium ion influx, which indicates that immune signals initiated on the plasma membrane or in cytoplasm converge at subsequent points. Despite significant breakthroughs in recent years in understanding the functioning of plant immune sensors, many important questions remain unanswered and require further research.

展开