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Research Article Free access | 10.1172/JCI110601
Department of Metabolism and Endocrinology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
Department of Pathology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
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Department of Metabolism and Endocrinology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
Department of Pathology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
Find articles by Smets, G. in: JCI | PubMed | Google Scholar
Department of Metabolism and Endocrinology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
Department of Pathology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
Find articles by Gepts, W. in: JCI | PubMed | Google Scholar
Department of Metabolism and Endocrinology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
Department of Pathology, Fakulteit Geneeskunde en Farmacie, Vrije Universiteit Brussel, 1090 Brussels, Belgium
Find articles by Pipeleers, D. in: JCI | PubMed | Google Scholar
Published July 1, 1982 - More info
Viable rat islet cells were used to detect islet cell surface antibodies (ICSA) in the sera of diabetic and control patients. ICSA were present in almost all recent-onset insulin-dependent diabetics younger than 30 yr (15/16); their incidence in other diabetics (6/22) was also higher than in normal controls (1/18) or in patients with autoimmune thyroiditis (1/12). The varying specificity of the ICSA for the different islet cell types led to the recognition of class I sera, whose ICSA bind exclusively to B cells, class II sera, binding only to A and pancreatic polypeptide (PP) cells and class III sera, reacting with the three islet cell types but not with D cells. Most recent-onset insulin-dependent diabetics younger than 30 contained class I-ICSA, which is consistent with an autoimmune basis of their disease and with an involvement of surface antibodies in the B cell destruction. The presence of class II ICSA in three older diabetics and in one normal control raises the question whether autoimmune reactions against A and PP cells exist and are associated with a distinct entity in islet disease.
It is concluded that the autoimmune form of diabetes mellitus represents a heterogeneous group, in which ICSA-positive patients can be distinguished on the basis of their ICSA-binding to one or more islet cell types.
Three techniques can be used for the further identification of circulating ICSA, namely binding experiments with purified A or B cells, electron microscopical analysis of ICSA-binding islet cells purified by fluorescence-activated cell sorting, and the immunocytochemical characterization of ICSA-positive cells.
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