Bacterial wilt disease caused by several Ralstonia species is one of the most destructive diseases in Solanaceae crops. Only a few functional resistance genes against bacterial wilt have been cloned so far. Here, we show that the broadly conserved type III secreted effector RipY is recognized by N. benthamiana immune system, leading to cell death induction, induction of defense-related gene expression, and restriction of bacterial pathogen growth. Using a multiplexed NbNLR-VIGS library, we identified a coiled-coil nucleotide-binding leucine-rich repeat receptor (CNL) required for recognition of RipY, which we named RESISTANCE TO RALSTONIA SOLANACEARUM RIPY (RRS-Y). Genetic complementation assays in RRS-Y silenced plants and in stable rrs-y knockout mutants demonstrate that RRS-Y is sufficient to activate RipY-induced cell death and RipY-induced immunity to R. pseudosolanacearum. RRS-Y function is dependent on the P-loop motif of the nucleotide-binding domain but independent on the characterized signaling components EDS1, ADR1, NRG1, or the NLR helpers NRC2, 3, and 4 in N. benthamiana. We further show that RRS-Y localization at the plasma membrane is mediated by two cysteine residues in the CC domain and is required for RipY recognition. RRS-Y also broadly recognizes RipY homologs across Ralstonia species. Lastly, we show that the C-terminal region of RipY is indispensable for RRS-Y activation. Altogether, our findings provide an additional effector/receptor pair system to deepen our understanding of CNL activation in plants.