Åke Lernmark received his medical degree from the University of Umeå in 1971. His early research in Umeå with Professor Bo Hellman led to the development of methods for the study of insulin secretion from microdissected islets and the discovery that extracts of the islet D cells inhibited insulin secretion, an important finding preceding the discovery of somatostatin as the D cell secretory product. Åke performed the first studies of the properties of free islet cell suspensions derived from isolated rodent islets. In 1974 he became Postdoctoral Fellow at the laboratory of Donald Steiner in the Department of Biochemistry at the University of Chicago. Here he scaled up islet cell preparations for first purification and characterization of islet cell membrane-fractions for development of islet cell surface antisera. In the late 70’s he applied the recently developed FACS techniques for sorting and characterizing of isolated islet beta, alpha and delta cell populations. Other important achievements during that period led to the discovery of islet cell surface antibodies in juvenile diabetics, which resulted in a landmark publication in the New Engl J Med in 1978.
In 1979 Åke Lernmark was appointed Director of Research at the Hagedorn Research Laboratories in Gentofte, Denmark. Åke was instrumental in making Hagedorn a world-leading laboratory and training center in diabetes research (so recognized by WHO). A number of key discoveries date to this time, among them the further dissection of the role of the HLA-D region in type 1 diabetes, revealing that HLA-DQ rather than DR confers disease susceptibility, and the key discovery (with Steinun Baekkeskov) of the 64K islet autoantigen as an excellent predictor of future type 1 diabetes. The 64K antigen was later shown by Åke Lernmark (with Allan E Karlsen) to be a hitherto unknown human islet isoform of glutamic acid decarboxylase (GAD65). These discoveries have represented real milestones in the history not only of diabetes research but also of clinical diabetes. Of particular importance was the demonstration that the -globulin fraction of 64K+ sera from t1d patients blocked the first phase of the glucose-stimulated insulin release, a finding later shown to have an important clinical counterpart.
In 1988 Åke Lernmark returned to the US to assume the Robert H. Williams Chair in Medicine at the University of Washington School of Medicine. Work in Seattle focused not only on the GAD65 discovery but also on the genetic dissection of autoimmune diabetes in the type 1 diabetes-like BB rat, demonstrating linkage with a lymphopenia gene on rat chromosome 4. Subsequent work by Åke Lernmark and his research fellows indicated that lymphopenia in the BB rat model is due to a mutation in a novel Immune-Associated Nucleotide (Ian) related gene, revealing a new family of anti-apoptotic factors, the GIMAP family.
The Lernmark-landmark studies described above represent only the tip of the iceberg of a bright and devoted scientist’s lifelong efforts to probe the genetics, immunology, environmental and other mechanisms responsible for type 1 diabetes. Åke Lernmark has become a distinguished leader in the international effort to achieve a better understanding and a cure for this major scourge of humanity. In pursuit of this goal he has trained and inspired several generations of physicians and scientists and developed international centers of excellence, taking advantage of unique resources that can provide valuable information and/or patient populations for study (e.g. numerous ICA, GADA and IA-2A workshops). A perusal of his Curriculum Vitae gives a taste of the ubiquity and scope of his manifold activities and responsibilities within the diabetes community.