Elevated temperatures suppress the biosynthesis and signaling of the plant defence hormone salicylic acid (SA) through downregulation of CBP60g, which encodes a master transcription factor of plant immunity. Constitutive CBP60g expression restores SA levels at elevated temperatures, showing its importance in plant immune resilience to a warming climate. However, the detailed mechanisms of how CBP60g restores immunity at higher temperatures is currently unknown. Here we illuminate CBP60g-mediated immune resilience through whole-scale changes in the plant’s protein and phosphorylation levels. After performing global proteome analysis of Arabidopsis thaliana plants infected with Pseudomonas syringae DC3000, we identified that infected wild-type Col-0 plants express more thermosensitive proteins when temperatures increase from 23°C to 28°C, compared to the thermoresilient CBP60g-overexpressing plants. In our thermoresilient CBP60g-overexpressing plants, we still observed a group of temperature-sensitive proteins, which could suggest novel thermosensing mechanisms upstream of CBP60g gene expression. One of these proteins was an H2A histone protein that was upregulated at warm temperatures. Functional analysis of mutants in the H2A protein H2A.Z resulted in loss of immune thermosensitivity. This result suggests that this temperature-sensitive histone H2A protein could potentially function as a central thermosensing mechanism leading to differential plant immune responsiveness under dynamically changing temperatures. Overall, this project provides a global proteome landscape underpinning plant immune responses in a changing environment, which revealed a histone-mediated immune thermosensing mechanism. This and other proteins are potential genetic engineering targets for crop disease prevention and climate resilience programs.