Summary The bacterial agent of citrus canker disease ( X anthomonas citri ssp. citri , X cc ) has caused tremendous economic losses to the citrus industry around the world. Pathogen‐associated molecular pattern ( PAMP )‐triggered immunity ( PTI ) is important to plant immunity. In this study, we compared the defence responses of citrus canker‐resistant and citrus canker‐susceptible genotypes to the X cc ‐derived PAMP flg22 ( Xflg22 ) by analysing the expression of 20 citrus defence‐associated genes. We showed that, in the most resistant genotype, ‘Nagami’ kumquat, there was significant induction of several defence genes ( EDS1 , NDR1 , PBS1 , RAR1 , SGT1 , PAL1 , NPR2 and NPR3 ) as early as 6 h and up to 72 h after X flg22 treatment. At the other end of the spectrum, highly susceptible ‘Duncan’ grapefruit showed no induction of the same defence genes, even 120 h after treatment. Citrus genotypes with partial levels of resistance showed intermediate levels of transcriptional reprogramming that correlated with their resistance level. X flg22 also triggered a rapid oxidative burst in all genotypes which was higher and accompanied by the induction of PTI marker genes ( WRKY22 and GST1 ) only in the more resistant genotypes. Pretreatment with X flg22 prior to X cc inoculation inhibited bacterial growth in kumquat, but not in grapefruit. A flagellin‐deficient X cc strain ( XccΔfliC ) showed greater growth increase relative to wild‐type X cc in kumquat than in grapefruit. Taken together, our results indicate that X flg22 initiates strong PTI in canker‐resistant genotypes, but not in susceptible ones, and that a robust induction of PTI is an important component of citrus resistance to canker.