Plant Stress Biology in a Warming World: Synergies in Abiotic and Biotic Adaptation

Rising temperatures do not act on plant disease through a single linear pathway. They simultaneously alter host immune competence, pathogen and pest performance, vector activity, phenology, tissue physiology and the environmental conditions that permit infection. This critical narrative review evaluates how warming reconfigures plant resistance and vulnerability across molecular, organismal and ecological scales. Literature published from 1 January 1990 to 30 June 2026 was selected through searches of major open scholarly sources, complemented by citation chaining and reference verification. The strongest mechanistic evidence shows that temperature can destabilise nucleotide-binding leucine-rich repeat receptor function, weaken salicylic-acid and N-hydroxypipecolic-acid defence programmes, suppress particular pattern-triggered responses and redirect growth-defence allocation. Yet these effects are neither universal nor uniformly deleterious. Moderate warming can favour selected pattern-triggered immune outputs, hypersensitive cell death can be uncoupled from pathogen restriction, antiviral RNA silencing may strengthen at higher temperature, root-zone warming can induce systemic protection, and natural genetic variation can preserve resistance under warm conditions. Antagonists also show heterogeneous thermal responses: bacterial virulence traits, fungal and oomycete infection risk, nematode resistance breakdown, insect metabolic demand and geographic redistribution are all temperature dependent, but their optima frequently differ from those of the host. Consequently, disease outcome is best understood as the overlap of host, antagonist and environment-specific thermal response curves rather than as a generic effect of warming. Major weaknesses in the evidence base include reliance on static growth-chamber temperatures, narrow genotype sampling, inconsistent definitions of heat stress, insufficient control of humidity and other covariates, and overreliance on symptoms or hypersensitive response as proxies for resistance. A translationally useful research agenda should prioritise thermally explicit phenotyping, multi-genotype and multi-pathogen validation, fluctuating temperature regimes, mechanistic separation of host and antagonist effects, and field testing of immune nodes that retain function under warming. The emerging goal is not constitutive defence, but temperature-resilient immunity that remains effective without unacceptable penalties to growth and yield.