Effector-triggered immunity

Alternatively, effector-triggered susceptibility (ETS) can occur if an effector protein can block the immune response triggered by pattern recognition receptors (PRR) and evade immunity, allowing the pathogen to propagate in the host.

[4] The basis of the ETI model lies in the gene-for-gene resistance hypothesis proposed by Harold Henry Flor in 1942.

[5] Flor proposed that plants may express resistance (R) proteins that recognise avirulence (Avr) proteins from pathogens, thus making them resistant to pathogen invasion.

His hypothesis has since been confirmed by identifying multiple Avr-R gene pairs.

[6] Some Avr proteins are direct ligands for receptors encoded by the R genes, such as the Leu-rich repeat receptors (LRRs).

The host cell detects the presence of the pathogen directly from the molecular patterns on the pathogen and indirectly through the damage caused to the host cell by the toxins generated by the pathogen.