Because of evidence that cow's milk intake can trigger diabetes in rodents, a study of diabetic children demonstrated antibodies to bovine serum albumin and a 17-amino-acid bovine serum albumin peptide (ABBOS). These antibodies would bind to a pancreatic beta-cell surface antigen. This study showed that diabetic patients had high serum concentrations of anti-BSA antibodies (IgA and IgG).

The presence of antibody (which means presence of antigen-specific B-cells) may signal the concomitant presence of antigen-specific cytotoxic T-lymphocytes, although these have not yet be demonstrated. The researchers suggest that ... "relevant clones (of lymphocytes) are continuously transferred from immature IgM-expressing B-cell compartments to pools of IgG-secreting or IgA secreting cells.... a slow inefficient process, consistent with the fact that clinical disease develops in only about 5 to 6 % of hosts with the relevant genetic predisposition."

An Australian study of children who developed diabetes found that children given cow’s milk formula in the first three months were 52% more likely to develop diabetes than those not fed milk. Breast fed infants had a 34% lower incidence of diabetes than formula fed infants. An Italian study showed that exposure to beta casein produced proliferation of T- lymphocytes from the blood of 51% of 41 insulin dependent diabetics.

The diabetes model of food-antigen triggered disease is an important immunological model of many unsolved diseases that appear to be "autoimmune". Food is an abundant source of protein antigens. A long-term, inefficient pathogenesis can produce target-organ damage, especially if the antigen challenge continues over many years.

Alternative explanations suggest that beta cells are attacked by cytotoxic T-cells after a virus infects them or by T-cells originally targeted on other cells infected by virus whose cell-surface antigens happen to resemble beta cell antigens. Coxsackie B viruses, for example

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Immunology Notes

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