Innate immunity plays a critical role in metabolic dysfunction-associated steatotic liver disease (MASLD), a prevalent liver condition linked to obesity and metabolic disorders. MASLD can progress from simple steatosis to liver inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. The pathogenesis of MASLD involves complex interactions between innate and adaptive immune responses, with pro-inflammatory cytokines, adipokines, and inflammasomes playing key roles in driving liver inflammation and fibrosis. Pro-inflammatory cytokines such as TNF-α and IL-1β contribute to the progression of MASLD by promoting inflammation and fibrosis. Adipokines like adiponectin also influence liver inflammation and insulin resistance, with lower levels observed in MASLD patients. Inflammasomes, particularly the NLRP3 inflammasome, are involved in the activation of pro-inflammatory cytokines and the progression of liver fibrosis. Various cell types, including macrophages, natural killer cells, and neutrophils, contribute to the inflammatory process in MASLD. The interplay between innate and adaptive immunity is crucial in the development and progression of MASLD. Targeting innate immune pathways may offer therapeutic strategies for managing MASLD and its complications. Understanding the mechanisms of innate immunity in MASLD is essential for developing effective treatments for this widespread condition.Innate immunity plays a critical role in metabolic dysfunction-associated steatotic liver disease (MASLD), a prevalent liver condition linked to obesity and metabolic disorders. MASLD can progress from simple steatosis to liver inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma. The pathogenesis of MASLD involves complex interactions between innate and adaptive immune responses, with pro-inflammatory cytokines, adipokines, and inflammasomes playing key roles in driving liver inflammation and fibrosis. Pro-inflammatory cytokines such as TNF-α and IL-1β contribute to the progression of MASLD by promoting inflammation and fibrosis. Adipokines like adiponectin also influence liver inflammation and insulin resistance, with lower levels observed in MASLD patients. Inflammasomes, particularly the NLRP3 inflammasome, are involved in the activation of pro-inflammatory cytokines and the progression of liver fibrosis. Various cell types, including macrophages, natural killer cells, and neutrophils, contribute to the inflammatory process in MASLD. The interplay between innate and adaptive immunity is crucial in the development and progression of MASLD. Targeting innate immune pathways may offer therapeutic strategies for managing MASLD and its complications. Understanding the mechanisms of innate immunity in MASLD is essential for developing effective treatments for this widespread condition.