Dr. Yaron Tomer is the Marilyn and Stanley M. Katz Dean at Albert Einstein College of Medicine and Chief Academic Officer at Montefiore Medicine.
He received his M.D. degree magna cum laude from the Sackler School of Medicine of Tel Aviv University and trained in Internal Medicine at Sheba Medical Center, Israel, and in Endocrinology at the Icahn School of Medicine at Mount Sinai in New York. Prior to joining Montefiore Einstein in March 2016, he was Chief of the Division of Endocrinology, Diabetes, and Bone Disease at Mount Sinai.
Dr. Tomer has served on the editorial boards of Endocrinology and The Journal of Clinical Endocrinology and Metabolism, among others. He is a member of the American Society for Clinical Investigation and a Fellow of the American College of Physicians. Dr. Tomer is the recipient of several prestigious awards, including the American Thyroid Association’s Sidney H. Ingbar Distinguished Lectureship Award, as well as its Van Meter Award.
Dr. Tomer’s research program focuses on the immunogenetic, epigenetic, and environmental mechanisms underlying thyroid autoimmunity, and type 1 diabetes, and on targeting these mechanisms in order to develop novel therapies. His group made several discoveries including identifying new genes and mechanisms underlying the strong association between type 1 diabetes and autoimmune thyroiditis; demonstrating that CD40 and thyroglobulin are major susceptibility genes for thyroid autoimmunity; identifying a unique amino acid variant in the peptide binding pocket of HLA-DR that is key for the development of thyroid autoimmunity; dissecting the epigenetic mechanisms by which polymorphisms in the thyroglobulin and TSHR genes interact with environmental agents (e.g. viruses) to trigger thyroid autoimmunity; and identifying a novel small molecule that can block antigen presentation in autoimmune thyroiditis.
- Genetic and epigenetic studies in thyroid autoimmunity
The Tomer lab mapped several susceptibility genes for autoimmune thyroid diseases (AITD) including CD40, thyroglobulin, and TSHR. Recent data suggest that variants in regulatory regions of some of these genes interact epigenetically with environmental factors (e.g., viral infections) to trigger disease. Current studies are using epigenomic screening, including whole genome methylation studies and ChiP-seq analyses to study these genetic-epigenetic interactions.
- Epigenetic studies in type 1 diabetes
Similar studies are utilizing epigenomic screening to analyze epigenetic interactions between known type 1 diabetes susceptibility genes and interferon alpha, a key cytokine secreted during viral infections.
- Translational studies in autoimmune thyroiditis (AITD) and type 1 diabetes
The Tomer lab discovered that the presence of arginine at position beta-74 of the peptide binding pocket of HLA-DR is critical for the development of AITD. This discovery led to a translational project aimed at blocking thyroid antigen presentation to T-cells by the arginine beta-74 HLA-DR peptide binding pocket as a potential therapy for AITD. Recently, the Tomer lab identified a small molecule, Cepharanthine, that can block antigen presentation and suppress AITD in mouse models. Similar studies are performed in type 1 diabetes where the aim is to block the HLA-DQ8 peptide binding pocket from presenting insulin peptides to T-cells as a novel strategy to treat autoimmune diabetes.
- Genetic and functional analyses of autoimmune polyglandular syndrome (APS) type 3
The co-occurrence of type 1 diabetes and autoimmune thyroiditis in the same individual is considered a variant of the APS type 3 syndrome. The Tomer lab discovered several new susceptibility genes for APS3. The lab is now analyzing the mechanisms by which these genes predispose to disease.
- The role of viruses in triggering autoimmune thyroiditis and type 1 diabetes
Certain infections, such as hepatitis C, are associated with autoimmune thyroiditis and diabetes. Current studies are aimed at dissecting the mechanisms by which interferon alpha, the primary cytokine secreted during viral infections, can trigger autoimmune thyroiditis and diabetes in genetically susceptible individuals.