In this episode of the College of Glycation, Professor Paul Reynolds examines how glycation helps drive autoimmune disease. Advanced glycation end-products bind the multi-ligand receptor RAGE, activating NF-κB and creating a self-amplifying inflammatory loop that recruits more immune cells. Elevated AGEs and reduced protective soluble RAGE appear consistently in rheumatoid arthritis, lupus, and related conditions. In type 1 diabetes, RAGE is expressed on both the attacking immune cells and the targeted beta cells, promoting aggressive responses while suppressing regulatory ones. Glycation also contributes to loss of self-tolerance by chemically modifying protein and DNA epitopes so that self-molecules no longer look like self. In multiple sclerosis lesions, methylglyoxal-derived AGEs accumulate in astrocytes while RAGE appears on nearby immune cells, feeding local neuroinflammation.

Dietary AGEs from high-heat cooking further raise the inflammatory burden and lower soluble RAGE. Practical levers include reducing dietary AGE load through gentler cooking methods, controlling blood glucose to limit endogenous glycation, and considering carnosine as a carbonyl scavenger. RAGE is a real contributor inside a redundant network rather than a single master switch, so the near-term wins remain the ones you control at the plate and in the kitchen.

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