Dr. Lernmark received his Dr. Med. from the University of Umeå, Umeå, Sweden in 1972. He has held faculty positions at the University of Umeå, the University of Chicago, the University of Lund, and the Karolinska Institute in Sweden. He has served as Director of Research at the Hagedorn Research Laboratory in Copenhagen. Dr. Lernmark was named the Robert H. Williams Professor of Medicine at the University of Washington in 1988 and joined the Department of Immunology in 1995.

Type 1 diabetes mellitus is the most common chronic disease among children and young adults. The disease develops because the immune system attacks the ß cells in the pancreatic islets. The role of autoantigens in the pathogenesis is of particular interest and both celluar and humoral mechanisms are studied. The Mr65,000 isoform of glutamate decarboxylase (GAD65) is a major autoantigen. Molecular cloning and site-directed mutagenesis is used in analyses of B and T cell function in humans. Quantitative and epitope-specific GAD65, insulin and IA-2 antibody assays combined with genetic markers are used to predict type 1 diabetes. The immunogenetics of HLA and other diabetes susceptibility genes is studied by molecular epidemiology by mapping diabetes genes in both family, and case-control studies as well as in prospective observtional clinical trials.

The spontaneously diabetic BB rat is studied to map and positionally clone diabetes genes to identify genetic mechanisms that control the development of autoimmune diabetes. A recessive gene for lymphopenia which is causing pancreatic islet and thyroid inflammation was mapped to rat chromosome 4 and by positional cloning lymphopenia was found to be due to a frameshift mutation in the GIMAP5 gene, which is controling T cell development. The research is also aimed at the development of novel therapies to halt autoimmune ß-cell destruction.