The plant immune system carries two interconnected tiers of receptors, one most frequently sensing molecules outside the cell and the other most frequently sensing molecules inside the cell. Both systems sense the intruder and respond by activating antimicrobial defenses in the infected cell and neighboring cells.  In some cases, defense-activating signals spread to the rest of the plant or even to neighboring plants.  The two systems detect different types of pathogen molecules and classes of plant receptor proteins.
The first tier is primarily governed by pattern recognition receptors that are activated by recognition of evolutionarily conserved pathogen or microbial–associated molecular patterns (PAMPs or MAMPs). Activation of PRRs leads to intracellular signaling, transcriptional reprogramming, and biosynthesis of a complex output response that limits colonization. The system is known as PAMP-triggered immunity or as pattern-triggered immunity (PTI).
The second tier, primarily governed by R gene products, is often termed effector-triggered immunity (ETI). ETI is typically activated by the presence of specific pathogen "effectors" and then triggers strong antimicrobial responses (see R gene section below).
In addition to PTI and ETI, plant defenses can be activated by the sensing of damage-associated compounds (DAMP), such as portions of the plant cell wall released during pathogenic infection.
Responses activated by PTI and ETI receptors include ion channel gating, oxidative burst, cellular redox changes, or protein kinase cascades that directly activate cellular changes (such as cell wall reinforcement or antimicrobial production), or activate changes in gene expression that then elevate other defensive responses.
Plant immune systems show some mechanistic similarities with the immune systems of insects and mammals, but also exhibit many plant-specific characteristics. The two above-described tiers are central to plant immunity but do not fully describe plant immune systems.  In addition, many specific examples of apparent PTI or ETI violate common PTI/ETI definitions, suggesting a need for broadened definitions and/or paradigms.
The term quantitative resistance (discussed below) refers to plant disease resistance that is controlled by multiple genes and multiple molecular mechanisms that each have small effects on the overall resistance trait.  Quantitative resistance is often contrasted to ETI resistance mediated by single major-effect R genes.