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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.
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.