Plants interact with a wide range of microbial pathogens, and have evolved a sophisticated defense system that recognizes pathogen molecules and activates specific defenses. Recent research has revealed that small-molecule hormones play a crucial role in regulating this defense network. These hormones cross-communicate in antagonistic or synergistic ways, allowing plants to finely regulate their immune response. Pathogens can manipulate these signaling pathways to evade host defenses by altering hormone homeostasis. Phytohormones, including abscisic acid (ABA), auxins, cytokinins, ethylene (ET), and gibberellins, regulate plant growth, development, and immunity. SA, JAs, and ET are key signals in plant immunity, while other hormones like ABA, auxins, and brassinosteroids also play roles. The interaction between these hormones allows plants to adapt to biotic and abiotic stresses, balancing growth and defense. The plant immune system includes both constitutive and inducible defenses. Constitutive defenses include physical barriers and antimicrobial compounds, while inducible defenses involve pattern recognition receptors (PRRs) and effector-triggered immunity (ETI). Pathogens can suppress these defenses by producing effectors that interfere with signaling pathways. Induced plant defense responses involve the activation of defense-related genes, such as those encoding pathogenesis-related (PR) proteins, and the production of antimicrobial secondary metabolites. These responses are regulated by phytohormones, with SA, JA, and ET playing central roles. Systemic acquired resistance (SAR) is a long-lasting, broad-spectrum defense that is activated by SA, while induced systemic resistance (ISR) is triggered by beneficial microbes and is regulated by JA and ET. Hormone signaling pathways interact in complex ways, with SA, JA, and ET being the primary signals. These pathways can antagonize or synergize, allowing plants to tailor their defenses to different attackers. For example, SA is important for biotrophic pathogen resistance, while JA and ET are more effective against necrotrophic pathogens. The interaction between these hormones is regulated by key signaling nodes such as NPR1, which plays a central role in SA signaling. Pathogens can manipulate these signaling pathways to suppress plant defenses. For example, P. syringae produces effectors that interfere with SA and JA signaling, while coronatine, a phytotoxin, mimics JA and suppresses SA-dependent defenses. Understanding these interactions is crucial for developing strategies to enhance plant immunity. The study of plant immunity has revealed the importance of hormone signaling in defense responses. The complex network of interactions between hormones allows plants to adapt to their environment and efficiently utilize resources. Future research should focus on integrating these findings into ecological contexts and using systems biology approaches to understand the emergent properties of plant immune signaling.Plants interact with a wide range of microbial pathogens, and have evolved a sophisticated defense system that recognizes pathogen molecules and activates specific defenses. Recent research has revealed that small-molecule hormones play a crucial role in regulating this defense network. These hormones cross-communicate in antagonistic or synergistic ways, allowing plants to finely regulate their immune response. Pathogens can manipulate these signaling pathways to evade host defenses by altering hormone homeostasis. Phytohormones, including abscisic acid (ABA), auxins, cytokinins, ethylene (ET), and gibberellins, regulate plant growth, development, and immunity. SA, JAs, and ET are key signals in plant immunity, while other hormones like ABA, auxins, and brassinosteroids also play roles. The interaction between these hormones allows plants to adapt to biotic and abiotic stresses, balancing growth and defense. The plant immune system includes both constitutive and inducible defenses. Constitutive defenses include physical barriers and antimicrobial compounds, while inducible defenses involve pattern recognition receptors (PRRs) and effector-triggered immunity (ETI). Pathogens can suppress these defenses by producing effectors that interfere with signaling pathways. Induced plant defense responses involve the activation of defense-related genes, such as those encoding pathogenesis-related (PR) proteins, and the production of antimicrobial secondary metabolites. These responses are regulated by phytohormones, with SA, JA, and ET playing central roles. Systemic acquired resistance (SAR) is a long-lasting, broad-spectrum defense that is activated by SA, while induced systemic resistance (ISR) is triggered by beneficial microbes and is regulated by JA and ET. Hormone signaling pathways interact in complex ways, with SA, JA, and ET being the primary signals. These pathways can antagonize or synergize, allowing plants to tailor their defenses to different attackers. For example, SA is important for biotrophic pathogen resistance, while JA and ET are more effective against necrotrophic pathogens. The interaction between these hormones is regulated by key signaling nodes such as NPR1, which plays a central role in SA signaling. Pathogens can manipulate these signaling pathways to suppress plant defenses. For example, P. syringae produces effectors that interfere with SA and JA signaling, while coronatine, a phytotoxin, mimics JA and suppresses SA-dependent defenses. Understanding these interactions is crucial for developing strategies to enhance plant immunity. The study of plant immunity has revealed the importance of hormone signaling in defense responses. The complex network of interactions between hormones allows plants to adapt to their environment and efficiently utilize resources. Future research should focus on integrating these findings into ecological contexts and using systems biology approaches to understand the emergent properties of plant immune signaling.