GLYCEMIA AND IMMUNE RESPONSES

Abstract

The intensity of experimental and clinical immune responses was correlated with the degree of glycemia of the reacting subject. Hyperglycemias resulting from overdosage with sugars, cortisol, adrenaline, or from diabetes inhibit the anaphylactoid reactions; anaphylaxis, and the tuberculin reaction; but potentiate infections. Hypoglycemias resulting from fasting, insulin and adrenalectomy potentiate the anaphylactoid reactions, anaphylaxis, and the tuberculin reaction; but inhibit infections. The hypothesis is proposed that hyperglycemia inhibits certain antigen-antibody combinations; this results in an inhibition of hypersensitivity, but an aggravation of infection.