The 12th International Immunology of Diabetes Workshop was held during April 1993 in Orlando, Florida, to review research progress since the 11th Immunology of Diabetes Workshop meeting in Nagasaki, Japan, one and a half years before. The NOD mouse may have as many as 10 susceptibility genes, including its novel IA major histocompatibility complex antigen and a defective interferon-γ receptor, whereas human IDDM is so far known to be encoded by cis and trans complementation products of certain DQ genes on chromosome 6q, and a gene in the insulin-like growth factor II region on chromosome 11p. A unique protein regulator of the × box promotor of the highly susceptible DQB1*0302 allele has also been found. Islet cell antibody negative siblings of IDDM patients appear to have lower than expected abilities to secrete insulin in response to intravenous glucose. Sera from patients before and/or after developing IDDM immunoprecipitate two native proteins of 64,000- and 38,000-Mr glutamic acid decarboxylase (GAD65) reacting to conformational epitopes. However, a multitude of other autoantibodies often reacting to denatured proteins through linear epitopes have also been identified. The first workshop for GAD antibody assays was successfully completed; however, the 38,000-Mr antigen has not yet been identified. Other autoantibodies reactive to gangliosides and to sulfatides continue to be reported. Insulitis has come to be recognized as a sometimes protective event. Protective insulitis predominates in older lesions. It can be induced by as disparate means as tuberculin antigen administration, by interleukin-4 treatments, by transfer of T-cell lines generated in autologous mixed lymphocyte responses, and by immunization to insulin B-chain, whereas oral islet cell antigens, such as insulin, can delay diabetes onset in the NOD mouse. Although Th2 cells may be important in protective insulitis, the NOD may actually have a deficiency of Th1 cells. Encapsulated islets can function for months after transplantation, whereas xenogeneic islet grafts appear to be rejected through a CD4+ T-cell–mediated mechanism like the pathogenic destruction of islets seen in NOD mice. We summarize a few of the meeting highlights.
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Perspectives in Diabetes|
August 01 1993
The 12th International Immunology and Diabetes Workshop: Orlando, Florida
Noel MacLaren;
Noel MacLaren
Department of Pathology and Laboratory Medicine, University of Florida College of Medicine
Gainesville, Florida
Barbara Davis Center for Childhood Diabetes, University of Colorado College of Medicine
Denver, Colorado
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Kevin Lafferty
Kevin Lafferty
Department of Pathology and Laboratory Medicine, University of Florida College of Medicine
Gainesville, Florida
Barbara Davis Center for Childhood Diabetes, University of Colorado College of Medicine
Denver, Colorado
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Address correspondence and reprint requests to Dr. Noel Maclaren, Box 100275, J. Hillis Miller Health Center, Gainesville, Florida 32610.
Diabetes 1993;42(8):1099–1104
Article history
Received:
May 07 1993
Revision Received:
May 21 1993
Accepted:
May 21 1993
PubMed:
8100786
Citation
Noel MacLaren, Kevin Lafferty; The 12th International Immunology and Diabetes Workshop: Orlando, Florida. Diabetes 1 August 1993; 42 (8): 1099–1104. https://doi.org/10.2337/diab.42.8.1099
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