Plant immunity and, in particular, immune responses induced by nucleotide-binding leucine-rich repeat receptors (NLRs) are often dampened above the optimal plant's growth range, but the underlying molecular mechanism remains elusive. N-terminal Toll/interleukin-1 receptor (TIR) domains are self-sufficient to trigger immune signaling. We showed that the conditional activation of two well-characterized TIR-containing NLRs (TNLs) or their corresponding TIR domains alone induce the same signaling route at permissive temperature (ENHANCED DISEASE SUSCEPTIBLITY 1 [EDS1]/helper NLRs that display an RPW8-like N-terminal CC