Glycemia and immune responses.
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.
D000707:Anaphylaxis; D000937:Antigen-Antibody Reactions; D001786:Blood Glucose; D003920:Diabetes Mellitus; D006801:Humans; D006943:Hyperglycemia; D006967:Hypersensitivity; D007003:Hypoglycemia; D007328:Insulin
D001786:Blood Glucose; D007328:Insulin
ANAPHYLAXIS; ANTIGEN-ANTIBODY REACTIONS; BLOOD SUGAR