ISSN:
1432-0428
Keywords:
Key words T-cell activation, T-cell memory, CD45 isoforms, HLA DR types, first degree relatives of diabetic patients.
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Type 1 (insulin-dependent) diabetes mellitus is associated with abnormalities of circulating lymphocyte subsets and autoantibodies. To investigate the prevalence of these in non-diabetic siblings and non-diabetic parents of children with Type 1 diabetes, we analysed T-cell subsets of function and activation in 31 families with an index case of Type 1 diabetes and related these to autoantibodies and HLA DR type. Using two and three colour cytofluorimetry, we studied total and activated (HLA-DR+) CD3+, CD4+, CD8+ lymphocytes and on CD4+ lymphocytes the CD45RA/RO “naive” and “memory” cell phenotypes. Diabetic children (mean duration of disease 3.1 years) had a reduced total lymphocyte count (p 〈0.05), their non-diabetic siblings a reduced CD4+ T-helper cell count (p 〈0.05), and their parents a reduced percentage and number of CD3+ T cells (p 〈0.01 and p 〈0.05) compared with age-matched control subjects. Diabetic children, their siblings and parents all had significantly increased levels of activated CD4+ T-helper cells (p 〈0.01, p 〈0.05 and p 〈0.01). In diabetic children and their siblings there was a significant over-expression of the CD45RO “memory” cell marker and significant under-expression of the CD45RA “naive” cell marker, whilst these were normal in the parents. Islet cell antibody positive diabetic children had significantly higher levels of CD45RO-expressing CD4+ lymphocytes than those who were islet cell antibody negative (p 〈0.05). Amongst the siblings and parents, possession of HLA-DR4 was associated with lower percentages of CD4+ and higher percentages of CD8+ T cells. These findings extend current knowledge about the role of immunoregulatory CD45RA/ RO cells in Type 1 diabetes. In addition, they demonstrate lymphocyte subset abnormalities in unaffected family members, some of which may be influenced by HLA DR alleles. [Diabetologia (1994) 37: 155–165]
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s001250050087
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