Sønderstrup, unpublished results), although they are perfectly capable of presenting these epitopes if they are provided as synthetic peptides. Further, these same human APCs can process and present other GAD65 epitopes normally to T cells that recognize these epitopes in the context of the DRB1* 0405 molecule (S. Parry and G. Sønderstrup, unpublished results). This result indicates that this is a selective epitope-specific phenomenon. The ability to eliminate potentially pathogenic T cells presented by coexpressed HLA class II molecules, HLA-DR or DQ, may be responsible for the disease-protective effect of the HLA-DRB1* 0403 allele and may therefore represent yet another mechanism for preventing autoimmunity in humans. The study of Wen et al.(10) and the results described above illustrate how HLA class II transgenic mice can provide a blueprint for unraveling DR/DQ allelic interactions in autoimmunity. This information should also provide new insight into pathogenesis and inspire novel strategies to prevent autoimmune disease.