Plants deal with a myriad of microbial attacks by employing a two-tiered innate immune system. The first tier is called pattern-triggered immunity (PTI), and the second tier is called effector-triggered immunity (ETI). PTI is triggered upon recognition of conserved microbial molecules known as microbe-associated molecular patterns (MAMPs) by plasmamembrane-localized pattern recognition receptors. Since pathogenic and nonpathogenic microbes often present common MAMPs, PTI could be activated by both types of microbes. Therefore, PTI should be tunable to alleviate fitness costs associated with unnecessary activation of immunity against nonpathogenic microbes and, at the same time, should be effective against pathogens that deploy virulence effectors to interfere with immune signaling components. Recent studies have shown that these properties of PTI are achieved via sophisticated networking of immune signaling components such as phytohormones and MAP kinases. However, pathogens exploit these regulatory interactions between immune signaling components to favor infection. Intriguing studies have recently demonstrated that plants can intercept pathogen exploitation of immune signaling networks during ETI, thereby reestablishing disease resistance. This review focuses on the structures and dynamics of immune signaling networks behind molecular interactions between plants and pathogens.