In plant-microbe interactions, a pathogenic microbe initially has to overcome preformed and subsequently induced plant defenses. One of the initial host-induced defense responses is microbe-associated molecular pattern (MAMP)-triggered immunity (MTI). Successful pathogens attenuate MTI by delivering various effectors that result in effector-triggered susceptibility and disease. However, some host plants developed mechanisms to detect effectors and can trigger effector-triggered immunity (ETI), thereby abrogating pathogen infection and propagation. Despite the wide acceptance of the above concepts, more and more accumulating evidence suggests that the distinction between MAMPs and effectors and MTI and ETI is often not given. This review discusses the complexity of MTI and ETI signaling networks and elaborates the current state of the art of defining MAMPs versus effectors and MTI versus ETI, but also discusses new findings that challenge the current dichotomy of these concepts.

中文翻译：

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植物免疫：MTI-ETI 模型及其他。

在植物-微生物相互作用中，病原微生物最初必须克服预先形成和随后诱导的植物防御。最初的宿主诱导的防御反应之一是微生物相关分子模式 (MAMP) 触发的免疫 (MTI)。成功的病原体通过传递导致效应物触发的易感性和疾病的各种效应物来减弱 MTI。然而，一些寄主植物开发了检测效应子的机制，可以触发效应子触发免疫 (ETI)，从而消除病原体的感染和繁殖。尽管上述概念已被广泛接受，但越来越多的证据表明，通常没有给出 MAMP 和效应器以及 MTI 和 ETI 之间的区别。