Intracellular calcium transients during plant-pathogen interactions are necessary early events leading to local and systemic acquired resistance. Salicylic acid, a critical messenger, is also required for both of these responses, but whether and how salicylic acid level is regulated by Ca(2+) signalling during plant-pathogen interaction is unclear. Here we report a mechanism connecting Ca(2+) signal to salicylic-acid-mediated immune response through calmodulin, AtSR1 (also known as CAMTA3), a Ca(2+)/calmodulin-binding transcription factor, and EDS1, an established regulator of salicylic acid level. Constitutive disease resistance and elevated levels of salicylic acid in loss-of-function alleles of Arabidopsis AtSR1 suggest that AtSR1 is a negative regulator of plant immunity. This was confirmed by epistasis analysis with mutants of compromised salicylic acid accumulation and disease resistance. We show that AtSR1 interacts with the promoter of EDS1 and represses its expression. Furthermore, Ca(2+)/calmodulin-binding to AtSR1 is required for suppression of plant defence, indicating a direct role for Ca(2+)/calmodulin in regulating the function of AtSR1. These results reveal a previously unknown regulatory mechanism linking Ca(2+) signalling to salicylic acid level.