The rationale: Activation of the immune response antagonizes plant growth and development in absence of pathogen, and such autoimmune phenotype is often suppressed by the elevation of ambient temperature. However, the molecular regulation of ambient temperature-sensitive intersection of immune response and growth is largely elusive. Methods: A genetic screen identified an Arabidopsis mutant, zed1-D, by its high temperature-dependent growth retardation. A combination of molecular, cytological and genetic approaches was used to investigate the molecular basis behind the temperature-sensitive growth and immune response in zed1-D. Key results: A dominant mutation in HOPZ-ETI-DEFICIENT 1 (ZED1) is responsible for a high temperature-dependent autoimmunity and growth retardation in the zed1-D. The autoimmune phenotype in the zed1-D is dependent on the HOPZ-ACTIVATED RESISTANCE 1 (ZAR1). ZED1 and some ZED1-related kinases (ZRKs) are induced by elevated temperature and function cooperatively to suppress the immune response by modulating the transcription of SUPPRESSOR OF NPR1-1 CONSTITUTIVE 1 (SNC1) in absence of pathogen. Main conclusion: Our data reveal a previously unidentified role of ZRKs in ambient temperature-sensitive immune response in absence of pathogen, and thus disclose a possible molecular mechanism underlying temperature-mediated intersection of immune response and growth in plants. Overall design: Compared the transcriptome of zed1-D with WT plants after being transferred from 18 into 28oC at different time points, 0h, 3h, 12h, and 48h.