Tomato (Solanum lycopersicum L.) is among the most economically important vegetable crops worldwide, yet its productivity and fruit quality are severely constrained by fungal pathogens employing biotrophic, necrotrophic, or hemibiotrophic lifestyles. Major pathogens-including Oidium neolycopersici, Alternaria solani, Botrytis cinerea, Fusarium oxysporum f. sp. lycopersici (FOL), Verticillium dahliae, and Phytophthora infestans-reshape host physiology through distinct infection strategies. This review synthesizes current knowledge on the early immune responses of tomato to fungal invasion, focusing on pattern-triggered immunity (PTI) initiated by pattern-recognition receptors (PRRs) and subsequent signaling via reactive oxygen species (ROS), Ca²⁺ transients, and MAPK cascades, as well as on effector-triggered immunity (ETI) mediated by intracellular R proteins. We compare host physiological outcomes across pathogen lifestyles, highlighting SA-dominant signaling against biotrophs versus JA/ET-dominant responses against necrotrophs, and the two-phased immune dynamics typical for hemibiotrophs. We further discuss effectors that suppress PTI and the circumstances under which hypersensitive-like cell death may paradoxically benefit necrotrophs (effector-triggered susceptibility). Finally, we outline integrative disease management directions-breeding for durable resistance, immune priming, biological control, and informed fungicide rotation-framed by a mechanistic understanding of PTI-ETI crosstalk in tomato. This mechanistic perspective provides a conceptual basis for developing resistant cultivars and robust integrated disease management strategies.