Animal and plant immune systems use intracellular nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) to detect pathogens, resulting in the activation of immune responses that are often associated with localized host cell death. Whereas vertebrate NLRs detect evolutionarily conserved molecular patterns and have undergone comparatively little copy number expansion, plant NLRs detect virulence factors that have often diversified in plant pathogen populations, and thus plant NLRs have been subject to parallel diversification. Plant NLRs sense the presence of virulence factors with enzymatic virulence activity often indirectly through their modification of host target proteins. By contrast, phytopathogenic virulence factors without enzymatic activity are usually recognized by NLRs directly by their structure. Structural and biochemical analyses have shown that both indirect and direct recognition of plant pathogens trigger the oligomerization of plant NLRs into active complexes. Assembly into three-layered ring-like structures has emerged as a common principle of NLR activation in plants and animals, but with distinct amino-terminal domains initiating different signalling pathways. Collectively, these analyses point to host cell membranes as a convergence point for activated plant NLRs and the disruption of cellular ion homeostasis as a possible major factor in NLR-triggered cell death signalling.

动植物免疫系统使用细胞内核苷酸结合寡聚化结构域 (NOD) 样受体 (NLR) 来检测病原体，从而激活通常与局部宿主细胞死亡相关的免疫反应。脊椎动物 NLRs 检测进化上保守的分子模式并且经历了相对较少的拷贝数扩张，而植物 NLRs 检测到植物病原体种群中经常多样化的毒力因子，因此植物 NLRs 受到平行多样化的影响。植物 NLR 通常通过对宿主靶蛋白的修饰间接感知具有酶毒力活性的毒力因子的存在。相比之下，没有酶活性的植物病原毒力因子通常通过其结构直接被 NLR 识别。结构和生化分析表明，植物病原体的间接和直接识别都会触发植物 NLR 寡聚化为活性复合物。组装成三层环状结构已成为植物和动物中 NLR 激活的常见原理，但具有不同的氨基末端结构域，可启动不同的信号通路。总的来说，这些分析指出宿主细胞膜是激活植物 NLR 的汇聚点，而细胞离子稳态的破坏可能是 NLR 触发的细胞死亡信号传导的主要因素。组装成三层环状结构已成为植物和动物中 NLR 激活的常见原理，但具有不同的氨基末端结构域，可启动不同的信号通路。总的来说，这些分析指出宿主细胞膜是激活植物 NLR 的汇聚点，而细胞离子稳态的破坏可能是 NLR 触发的细胞死亡信号传导的主要因素。组装成三层环状结构已成为植物和动物中 NLR 激活的常见原理，但具有不同的氨基末端结构域，可启动不同的信号通路。总的来说，这些分析指出宿主细胞膜是激活植物 NLR 的汇聚点，而细胞离子稳态的破坏可能是 NLR 触发的细胞死亡信号传导的主要因素。