Redox status and immune function in type I diabetes families

SUMMARY Because abnormalities in redox balance cluster in type I diabetes families and the intracellular thiol redox status seems to modulate immune function, we aimed to investigate the relationship between oxidative stress and immunological features. We measured oxidative markers, serum proinflammatory cytokines, soluble cytokine receptors and subsets of peripheral blood lymphocytes (by varying combinations of CD4, CD8, CD23 or low‐affinity IgE receptor, and CD25 or IL‐2 receptor) from 38 type I patients, 76 low‐risk (i.e. without underlying islet autoimmunity) non‐diabetic first‐degree relatives of diabetic patients, and 95 healthy subjects. In type I diabetes families, protein and lipid oxidation was confirmed by the presence of reduced sulphhydryl groups, increased advanced oxidation protein products, and increased plasma and erythrocyte malondialdehyde. Relatives had decreased counts of monocytes, of cells co‐expressing CD23 and CD25 and of CD25+ cells in peripheral blood. Patients with TIDM had similar defects and, in addition, showed decreased counts of peripheral CD4+CD8+ lymphocytes and increased serum levels of soluble receptors for interleukin (IL)‐6 and IL‐2. Abnormal indicators of oxidative stress were related in part to immune abnormalities. In the whole study group, we found a correlation (multiple R 0·5, P