Lectins stimulate class II HLA antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells.9 The islet cell determinant to which cytotoxic autoantibodies bind in insulin dependent diabetes mellitus is the disaccharide N-acetyl lactosamine,10 which must bind tomato lectin if present and probably also the lectins of wheat, potato, and peanuts. This would result in islet cells expressing both class II HLA antigens and foreign antigen together—a sitting duck for autoimmune attack. Certain foods (wheat, soya) are indeed diabetogenic in genetically susceptible mice.11 Insulin dependent diabetes therefore is another potential lectin disease and could possibly be prevented by prophylactic oligosaccharides.
Another suspect lectin disease is rheumatoid arthritis. The normal human IgG molecule possesses carbohydrate side chains, which terminate with galactose. In rheumatoid arthritis much of the galactose is missing, so that the subterminal sugar—N-acetyl glucosamine—is exposed instead. These deficient IgG molecules feature strongly in the circulating immune complexes that cause fever and symptoms.12 In diet responsive rheumatoid arthritis one of the commonest trigger foods is wheat, and wheat lectin is specific for N-acetyl glucosamine—the sugar that is normally hidden but exposed in rheumatoid arthritis. This suggests that N-acetyl glucosamine oligomers such as chitotetraose (derived from the chitin that forms crustacean shells) might be an effective treatment for diet associated rheumatoid arthritis. Interestingly, the health food trade has already siezed on N-acetyl glucosamine as an antiarthritic supplement.
Among the effects observed in the small intestine of lectin fed rodents is stripping away of the mucous coat to expose naked mucosa and overgrowth of the mucosa by abnormal bacteria and protozoa.14 Lectins also cause discharge of histamine from gastric mast cells,15 which stimulates acid secretion. So the three main pathogenic factors for peptic ulcer—acid stimulation, failure of the mucous defence layer, and abnormal bacterial proliferation (Helicobacter pylori) are all theoretically linked to lectins.