The regulation of pattern recognition receptor (PRR) signalling in plants is a critical aspect of plant innate immunity. PRRs, located at the cell surface, recognize conserved microbial features such as pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), initiating immune responses that deter infection. PRRs are part of multimeric complexes at the plasma membrane, which recruit cytoplasmic kinases to activate downstream signalling components. Ligand binding triggers a series of phosphorylation events that activate immune responses, including reactive oxygen species (ROS) production, calcium influx, and transcriptional reprogramming. However, excessive immune activation can be detrimental, so plants have evolved complex negative regulatory systems to maintain homeostasis. Pathogens can subvert this by secreting effectors that mimic host negative regulators. PRRs are classified based on their ligand-binding ectodomains, such as LRR-containing PRRs, LysM-containing PRRs, lectin-type PRRs, and EGF-like PRRs. These PRRs interact with regulatory receptor kinases and RLCKs to transduce signals. The activation of PRR complexes involves dynamic interactions with co-receptors, leading to the initiation of immune signalling. For example, the Arabidopsis LRR-receptor kinase FLS2 interacts with BAK1 to initiate immune responses upon flagellin recognition. Similarly, CERK1 interacts with LysM-containing PRRs to activate immune signalling. RLCKs, such as BIK1, play a key role in PRR-mediated immunity by phosphorylating downstream components like RBOHD, which is crucial for ROS production and stomatal closure. MAPK cascades are also involved in transcriptional reprogramming and immune responses. Negative regulation of PRR-mediated immunity is achieved through various mechanisms, including pseudokinases, protein phosphatases, and ubiquitin-mediated degradation. These mechanisms ensure that immune responses are tightly controlled to prevent autoimmunity and maintain cellular homeostasis. Hormones such as salicylic acid, jasmonic acid, and ethylene play important roles in regulating immune responses. Salicylic acid enhances PAMP-triggered responses, while jasmonic acid can suppress them. Ethylene promotes FLS2 transcription and interacts with other hormones to modulate immune responses. Additionally, endogenous peptides like PSK α and PSY1 can negatively regulate PTI responses, creating a feedback loop that opposes immunity and promotes growth. The complexity of PRR-mediated immunity highlights the need for further research to understand the molecular mechanisms underlying immune signalling. Future studies should focus on elucidating the interactions between different regulatory mechanisms, the role of post-translational modifications in PRR signalling, and the integration of hormonal and peptide signals in immune responses. Understanding these processes will be crucial for developing strategies to enhance disease resistance in crops.The regulation of pattern recognition receptor (PRR) signalling in plants is a critical aspect of plant innate immunity. PRRs, located at the cell surface, recognize conserved microbial features such as pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), initiating immune responses that deter infection. PRRs are part of multimeric complexes at the plasma membrane, which recruit cytoplasmic kinases to activate downstream signalling components. Ligand binding triggers a series of phosphorylation events that activate immune responses, including reactive oxygen species (ROS) production, calcium influx, and transcriptional reprogramming. However, excessive immune activation can be detrimental, so plants have evolved complex negative regulatory systems to maintain homeostasis. Pathogens can subvert this by secreting effectors that mimic host negative regulators. PRRs are classified based on their ligand-binding ectodomains, such as LRR-containing PRRs, LysM-containing PRRs, lectin-type PRRs, and EGF-like PRRs. These PRRs interact with regulatory receptor kinases and RLCKs to transduce signals. The activation of PRR complexes involves dynamic interactions with co-receptors, leading to the initiation of immune signalling. For example, the Arabidopsis LRR-receptor kinase FLS2 interacts with BAK1 to initiate immune responses upon flagellin recognition. Similarly, CERK1 interacts with LysM-containing PRRs to activate immune signalling. RLCKs, such as BIK1, play a key role in PRR-mediated immunity by phosphorylating downstream components like RBOHD, which is crucial for ROS production and stomatal closure. MAPK cascades are also involved in transcriptional reprogramming and immune responses. Negative regulation of PRR-mediated immunity is achieved through various mechanisms, including pseudokinases, protein phosphatases, and ubiquitin-mediated degradation. These mechanisms ensure that immune responses are tightly controlled to prevent autoimmunity and maintain cellular homeostasis. Hormones such as salicylic acid, jasmonic acid, and ethylene play important roles in regulating immune responses. Salicylic acid enhances PAMP-triggered responses, while jasmonic acid can suppress them. Ethylene promotes FLS2 transcription and interacts with other hormones to modulate immune responses. Additionally, endogenous peptides like PSK α and PSY1 can negatively regulate PTI responses, creating a feedback loop that opposes immunity and promotes growth. The complexity of PRR-mediated immunity highlights the need for further research to understand the molecular mechanisms underlying immune signalling. Future studies should focus on elucidating the interactions between different regulatory mechanisms, the role of post-translational modifications in PRR signalling, and the integration of hormonal and peptide signals in immune responses. Understanding these processes will be crucial for developing strategies to enhance disease resistance in crops.