Plant intracellular immune receptors, primarily nucleotide-binding, leucine-rich repeat proteins (NLRs), can detect virulence proteins (effectors) from pathogens and activate NLR-triggered immunity (NTI). Recently, ‘sensor’ NLRs have been reported to function with ‘helper’ NLRs to activate immune responses. We investigated the role of two helper NLRs, Nrc2 (NLR required for cell death 2) and Nrc3, on immunity in tomato to the bacterial pathogenPseudomonas syringaepv.tomato(Pst) mediated by the sensor NLR Prf and the Pto kinase. Loss-of-function mutations in bothNrc2andNrc3completely compromised Prf/Pto-mediated NTI toPstcontaining the cognate effectors AvrPto and AvrPtoB. Annrc3mutant showed intermediate susceptibility between wild-type tomato plants and aPrfmutant, while annrc2mutant developed only mild disease symptoms. These observations indicate that Nrc2 and Nrc3 act additively to contribute to Prf/Pto-mediated immunity. We also examined at what point Nrc2 and Nrc3 act in the Prf/Pto-mediated immune response. In thenrc2/3mutant, programmed cell death (PCD) normally induced by constitutively-active variants of AvrPtoB, Pto or Prf was abolished, but that induced by M3Kα or Mkk2 was not. PCD induced by a constitutively active variant of Nrc3 was also abolished in aNicotiana benthamianaline with reduced expression ofPrf. MAPK activation triggered by expression of AvrPto in the wild-type Pto-expressing tomato plants was completely abolished in thenrc2/3 mutant. These results indicate that Nrc2 and Nrc3 act in concert with Prf/Pto and upstream of MAPK signaling. Nrc2 and Nrc3 were not required for the HR triggered by Ptr1, another sensor NLR mediatingPstresistance, although these helper NLRs do appear to be involved in resistance to certainPstrace 1 strains.