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Phytophthora pathogens secrete a large arsenal of effectors that manipulate host processes to create an environment conducive to pathogen colonization.However,the underlying mechanisms by which Phytophthora effectors manipulate host plant cells still remain largely unclear.In this study,we report that PcAvr3a12,a Phytophthora capsici RXLR effector and a member of the Avr3a effector family,suppresses plant immunity by targeting and inhibiting host plant peptidyl-prolyl cis-trans isomerase (PPlase).Overexpression of PcAvr3a12 inArabidopsis thaliana enhanced plant susceptibility to P.capsici.FKBP15-2,an endoplasmic reticulum (ER)-Iocalized protein,was identified as a host target of PcAvr3a12 during early P.capsici infection.Analyses ofA.thaliana T-DNA insertion mutant (fkbp15-2),RNAi,and overexpression lines consistently showed that FKBP15-2 positively regulates plant immunity in response to Phytophthora infection.FKBP15-2 possesses PPlase activity essential for its contribution to immunity but is directly suppressed by PcAvr3a12.Interestingly,we found that FKBP15-2 is involved in ER stress sensing and is required for ER stress-mediated plant immunity.Taken together,these results suggest that P.capsici deploys an RXLR effector,PcAvr3a12,to facilitate infection by targeting and suppressing a novel ER-Iocalized PPlase,FKBP15-2,which is required for ER stress-mediated plant immunity.