Showing papers by "Elmar Jaeckel published in 2004"
TL;DR: It is shown that unlike tolerance to glutamic acid decarboxylase, tolerance to transgenically overexpressed preproinsulin 2 substantially reduced the onset and severity of type 1 diabetes in nonobese diabetic mice.
Abstract: Although autoimmune diseases can be initiated by immunization with a single antigen, it is not clear whether a single self antigen is essential for the initiation and, perhaps, the perpetuation of spontaneous autoimmunity. Some studies have suggested that insulin may represent an essential autoantigen in type 1 diabetes. Here we show that unlike tolerance to glutamic acid decarboxylase, tolerance to transgenically overexpressed preproinsulin 2 substantially reduced the onset and severity of type 1 diabetes in nonobese diabetic mice. However, some mice still developed type 1 diabetes, suggesting that insulin is a key, but not absolutely essential, autoantigen. The results are consistent with the idea that the human IDDM2 locus controls susceptibility to type 1 diabetes by regulating intrathymic preproinsulin expression.
129 citations
5 citations
TL;DR: On page 1034, line 12, reference 40 should be reference 40 and the reference number should be 37 because the author did not know that reference 37 was in use.
Abstract: Corrigendum: Recessive tolerance to preproinsulin 2 reduces but does not abolish type 1 diabetes
1 citations