CD36 in asthma: from a candidate immunometabolic checkpoint to genetic susceptibility

Asthma arises from complex interactions between genetic susceptibility and environmental exposure, yet the molecular pathways linking these processes remain incompletely understood. Recent human genetic studies have implicated CD36, a multifunctional class B scavenger receptor, in asthma risk, renewing interest in its immunological functions beyond lipid transport. Accumulating evidence suggests that CD36 influences multiple stages of disease pathogenesis, including allergen recognition and uptake, immune-cell activation and lipid-dependent metabolic adaptation. The identification of the asthma-protective variant rs75326924 has further connected CD36 biology to human disease and provided a genetic framework for mechanistic investigation. At the same time, emerging studies suggest that CD36 integrates extracellular lipid cues with intracellular immunometabolic programs that support persistent inflammatory responses, thereby providing a potential mechanistic link between environmental exposure and disease susceptibility. In this review, we discuss current evidence linking CD36 to asthma susceptibility and pathogenesis, evaluate the mechanistic basis of its immunological activities and discuss its potential as a biomarker and therapeutic target. We propose that CD36 represents a candidate immunometabolic checkpoint at the intersection of environmental sensing, metabolic regulation and genetic risk.