Alterations in lymphocyte subpopulations in type 1 (insulin-dependent) diabetes mellitus: exploration of possible mechanisms and relationships to autoimmune phenomena

✍ Scribed by K. C. Herold; A. Huen; L. Gould; H. Traisman; A. H. Rubenstein

• Publisher: Springer
• Year: 1984
• Tongue: English
• Weight: 387 KB
• Volume: 27
• Category: Article
• ISSN: 0012-186X
• DOI: 10.1007/bf00275660

✦ Synopsis

Previous studies have shown a variety of immunological abnormalities in Type 1 (insulin-dependent) diabetes, including disturbances in peripheral lymphocytes and anti-lymphocyte antibodies. We measured subsets of T and natural killer cells with monoclonal antibodies in patients with diabetes, and also assayed for anti-lymphocyte antibodies using dual colour immunofluorescence and flow cytometry. We found a significant decrease in numbers of Leu 3a (helper/inducer) cells in Type 1 diabetic patients of recent onset and intermediate levels in patients with longer duration of the disease. Leu 4 (pan T cell) levels were reduced in Type 1 diabetic patients of more than 4 months duration. Leu 7 (natural killer cells) were increased in Type 2 (non-insulin-dependent) diabetic patients. Individual Type 1 diabetic patients of recent onset showed low levels of Leu 7 and 11 a (natural killer cell) levels with normal 3a levels. Autoantibodies against Leu 3a + cells were present in higher titres in the Type 1 diabetic patients of recent onset than in control subjects. We conclude: (1) Leu 3a cells may be decreased in Type 1 diabetic patients of recent onset and return to normal with time; (2) low numbers of Leu 7 and 11a cells with normal numbers of Leu 3a may be seen in some Type 1 diabetic patients of recent onset, which may help explain previous reports of decreased suppressor cells; (3) Leu 7 levels may be increased in Type 2 diabetes; (4) autoantibodies against Leu 3a + peripheral lymphocytes may be seen in Type 1 diabetic patients of recent onset. These appear to be a marker of autoimmune phenomena rather than immunological mediators.