NOD-like receptors (NLRs) are central components of the plant immune system. L6 is a Toll/interleukin-1 receptor (TIR) domain-containing NLR from flax, which confers immunity to strains of the flax rust fungus expressing the effector AvrL567. Comparison of L6 to the weaker allele L7 identified two polymorphic regions in the TIR and the nucleotide binding (NB) domains that control both effector ligand-dependent and -independent cell death signaling as well as nucleotide binding to the receptor. These findings suggest that a negative functional interaction between the TIR and NB domains hold L7 in an inactive/ADP-bound state more tightly than L6, hence decreasing its capacity to adopt the active/ATP-bound state and explaining its weaker activity in planta. Furthermore, yeast-2-hybrid assays detected binding between AvrL567 and L6 or L7 variants that can activate a cell death signaling response, but not with those that are signaling inactive and have a more stable ADP-bound state. This finding differs from current models, which predict that effectors bind to inactive receptors and trigger their activation. Based on the correlation between nucleotide binding, effector interaction and immune signaling properties of L6/L7 variants, we propose an equilibrium-based switch model. In this model, the NLR exists in an equilibrium between "on" and "off" states and effector binding to the "on" state stabilizes this conformation, thereby shifting the equilibrium towards the active form of the receptor to trigger defense signaling.