THE 12TH INTERNATIONAL IMMUNOLOGY AND DIABETES WORKSHOP - ORLANDO, FLORIDA

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 suscepti bility genes, including its novel IA major histocompatibility complex antigen and a defective interferon-gamma receptor, whereas human IDDM is so far known to be encoded by cis and trans complementation product s of certain DO genes on chromosome 6q, and a gene in the insulin-like growth factor II region on chromosome 11p. A unique protein regulator of the X box promotor of the highly susceptible DQB10302 allele has also been found. Islet cell antibody negative siblings of IDDM patient s appear to have lower than expected abilities to secrete insulin in r esponse to intravenous glucose. Sera from patients before and/or after developing IDDM immunoprecipitate two native proteins of 64,000- and 38,000-M(r) glutamic acid decarboxylase (GAD65) reacting to conformati onal epitopes. However, a multitude of other autoantibodies often reac ting to denatured proteins through linear epitopes have also been iden tified. The first workshop for GAD antibody assays was successfully co mpleted; however, the 38,000-M(r) antigen has not yet been identified. Other autoantibodies reactive to gangliosides and to sulfatides conti nue 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 adminis tration, by interleukin-4 treatments, by transfer of T-cell lines gene rated in autologous mixed lymphocyte responses, and by immunization to insulin B-chain, whereas oral islet cell antigens, such as insulin, c an delay diabetes onset in the NOD mouse. Although Th2 cells may be im portant in protective insulitis, the NOD may actually have a deficienc y of Th1 cells. Encapsulated islets can function for months after tran splantation, whereas xenogeneic islet grafts appear to be rejected thr ough a CD4+ T-cell-mediated mechanism like the pathogenic destruction of islets seen in NOD mice. We summarize a few of the meeting highligh ts.