Specific immunoregulation abnormality in insulin-dependent diabetes mellitus.
We evaluated antigen-nonspecific (Con A) and antigen-specific (islet cell) activation of suppressor cell function in 11 IDD patients. Compared with healthy controls, IDD was associated with both antigen-specific (n = 11, p less than 0.01) and nonspecific (n = 6, p less than 0.03) suppressor cell hypofunction. The specific defect was not present in NIDD patients and correlated negatively with the duration of the disease (r = -0.6, p less than 0.05). No relationship was found between the degree of specific suppressor cell dysfunction and diabetic control as assessed by glycosylated hemoglobin, plasma glucose values, insulin-binding capacity, or C-peptide determinations. Plasma from IDD lacked anti-suppressor cell activity. Low levels of circulating immune complexes were detected in IDD patients whose disease duration was 1 month or less. Specific suppressor cell hypofunction and/or enhanced helper cell activity in early stages of IDD could be contributing to the formation of islet cell autoantibodies, immune complexes, islet cell injury, and the diabetic state.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000276:immunology; D000936:Antigen-Antibody Complex / Q000032:analysis; D001786:Blood Glucose; D002648:Child; D003208:Concanavalin A / Q000494:pharmacology; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology*; D005260:Female; D006454:Hemoglobins / Q000032:analysis; D006648:Histocompatibility; D006801:Humans; D007328:Insulin / Q000378:metabolism; D008213:Lymphocyte Activation; D008875:Middle Aged; D010179:Pancreas / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000276:immunology*
D000911:Antibodies, Monoclonal; D000936:Antigen-Antibody Complex; D001786:Blood Glucose; D006454:Hemoglobins; D007328:Insulin; D003208:Concanavalin A