Editorial Volume 11, Issue 7 pp 1900—1902

IgE, α-Gal and atherosclerosis

Figure 1. Proposed model to explain the relationship between IgE sensitization to α-Gal and CAD. The hypothesized relationship involves an interaction between a specific IgE immune response to α-Gal and dietary consumption of α-Gal-bearing glycolipids. (A) Representative depiction of a glycolipid with an α-Gal epitope. Such glycolipids are present in red blood cell membranes, muscle, fat and secretions of non-primate mammals. (B) Dietary lipids are absorbed through the intestinal epithelium and packaged into lipoprotein particles. Initially this involves chylomicrons before passing to smaller particles such as LDL or HDL that can subsequently deliver α-Gal epitopes to peripheral tissue where mast cells reside. Importantly, this can include mast cells within atherosclerotic plaques. (C) Specific IgE are bound to mast cells, including IgE specific to α-Gal, in subjects who are sensitized to the oligosaccharide, and thus α-Gal from dietary exposure could bind to and activate signal transduction via the high-affinity IgE receptor (Fc εR1). Relatively low levels of α-Gal exposure may be insufficient to induce mast cell degranulation, and thus not lead to overt allergic symptoms such as hives or anaphylaxis, but could nonetheless lead to chronic mast cell activation and pro-inflammatory effects.