Figure 2.

Sphingomyelin regulates CD1d access to potentially agonistic lipids. (A) In the absence of sphingomyelin, lipid antigens are free to access CD1d present in antigen-presenting cells (APCs), binding to iNKT cell TCR and leading to cell activation. (B) In cases of ASM deficiency, excess sphingomyelin binds to CD1d on APCs, preventing the binding of lipid antigens, and, as a consequence, leads to impediment of iNKT cell activation.