Plant cell walls are essential for plant adaptation to environmental conditions and play a key role in disease resistance. These dynamic structures can be altered in response to environmental challenges and developmental cues, leading to the release of wall molecules like carbohydrates (glycans) that function as damage-associated molecular patterns (DAMPs). DAMPs are recognized by pattern recognition receptors (PRRs) to activate pattern-triggered immunity (PTI) and disease resistance. Similarly, glycans from microbial walls are recognized as microbe-associated molecular patterns (MAMPs) by specific PRRs, triggering PTI responses. Recent studies have identified numerous oligosaccharide DAMPs/MAMPs, but the structural mechanisms underlying glycan recognition by plant PRRs remain limited. Current knowledge is mainly focused on LysM-PRR family receptors, which recognize chitooligosaccharides from fungi and lipo-chitooligosaccharides from bacteria. Other PRR families, such as LRR-MAL RKs, CrRLK1L, and wall-associated kinases, have also been implicated in oligosaccharide recognition. Understanding these mechanisms could lead to the development of sustainable, glycan-based crop protection solutions. Plant cell walls are composed of diverse polysaccharides, including cellulose, pectins, and hemicelluloses, with complex structures that vary between plant species and tissues. These structures are crucial for mechanical support, cell growth, and differentiation. Pathogens must overcome these barriers, often using cell wall-degrading enzymes (CWDEs) to break down walls and access plant tissues. The modification of cell wall integrity or composition can trigger plant defense responses, as seen in mutants with altered cell wall components. For example, Arabidopsis mutants with impaired cellulose synthesis show enhanced resistance to certain pathogens. Similarly, changes in pectin content or structure affect resistance to various pathogens. Callose, a β-1,3-D-glucan, plays a significant role in plant defense by forming papillae at sites of fungal penetration, hindering pathogen entry. Mutants with altered callose deposition exhibit different resistance patterns. Additionally, modifications in cell wall components like AGPs, lignin, and hemicelluloses influence disease resistance. For instance, reduced lignin content increases susceptibility to pathogens, while increased lignin content enhances resistance. Hormonal signaling pathways, such as those involving jasmonic acid (JA), ethylene (ET), and abscisic acid (ABA), are also involved in regulating plant defense responses. The release of DAMPs from cell walls can activate PTI, leading to enhanced disease resistance. These DAMPs, such as oligogalacturonides (OGs) and xyloglucans, are recognized by PRRs, triggering immune responses. The homeostasis of DAMPs/MAMPs is crucial for modulating immune responses, as excessive accumulation can lead to hyper-immPlant cell walls are essential for plant adaptation to environmental conditions and play a key role in disease resistance. These dynamic structures can be altered in response to environmental challenges and developmental cues, leading to the release of wall molecules like carbohydrates (glycans) that function as damage-associated molecular patterns (DAMPs). DAMPs are recognized by pattern recognition receptors (PRRs) to activate pattern-triggered immunity (PTI) and disease resistance. Similarly, glycans from microbial walls are recognized as microbe-associated molecular patterns (MAMPs) by specific PRRs, triggering PTI responses. Recent studies have identified numerous oligosaccharide DAMPs/MAMPs, but the structural mechanisms underlying glycan recognition by plant PRRs remain limited. Current knowledge is mainly focused on LysM-PRR family receptors, which recognize chitooligosaccharides from fungi and lipo-chitooligosaccharides from bacteria. Other PRR families, such as LRR-MAL RKs, CrRLK1L, and wall-associated kinases, have also been implicated in oligosaccharide recognition. Understanding these mechanisms could lead to the development of sustainable, glycan-based crop protection solutions. Plant cell walls are composed of diverse polysaccharides, including cellulose, pectins, and hemicelluloses, with complex structures that vary between plant species and tissues. These structures are crucial for mechanical support, cell growth, and differentiation. Pathogens must overcome these barriers, often using cell wall-degrading enzymes (CWDEs) to break down walls and access plant tissues. The modification of cell wall integrity or composition can trigger plant defense responses, as seen in mutants with altered cell wall components. For example, Arabidopsis mutants with impaired cellulose synthesis show enhanced resistance to certain pathogens. Similarly, changes in pectin content or structure affect resistance to various pathogens. Callose, a β-1,3-D-glucan, plays a significant role in plant defense by forming papillae at sites of fungal penetration, hindering pathogen entry. Mutants with altered callose deposition exhibit different resistance patterns. Additionally, modifications in cell wall components like AGPs, lignin, and hemicelluloses influence disease resistance. For instance, reduced lignin content increases susceptibility to pathogens, while increased lignin content enhances resistance. Hormonal signaling pathways, such as those involving jasmonic acid (JA), ethylene (ET), and abscisic acid (ABA), are also involved in regulating plant defense responses. The release of DAMPs from cell walls can activate PTI, leading to enhanced disease resistance. These DAMPs, such as oligogalacturonides (OGs) and xyloglucans, are recognized by PRRs, triggering immune responses. The homeostasis of DAMPs/MAMPs is crucial for modulating immune responses, as excessive accumulation can lead to hyper-imm