Einstein/Montefiore Department of Medicine

Department Faculty

Dr. Yaron Tomer, M.D.

Yaron Tomer, M.D.

Professor, Department of Medicine (Endocrinology)

Professor, Department of Microbiology & Immunology

Chair, Department of Medicine

Anita and Jack Saltz Chair in Diabetes Research

Areas of Research: 1. Immunogenetics of autoimmune Thyroid disease (AITD) and type 1 diabetes (T1D) 2.Gene-environment interactions in AITD and T1D 3. Epigenetics of AITD and T1D 4. Environmental chemical triggers of T1D

Professional Interests

Dr. Yaron Tomer is the Anita and Jack Saltz Chair in Diabetes Research and Professor and University Chair of the Department of Medicine at Albert Einstein College of Medicine and Montefiore Health System. He received his MD 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 Einstein/Montefiore in March 2016, he was Chief of the Division of Endocrinology, Diabetes and Bone Disease at Mount Sinai.

Dr. Tomer 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. He is the recipient of several prestigious awards, including the American Thyroid Association’s Van Meter Award and the Abbot Thyroid Clinical Research Mentor 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; demonstrating that the hepatitis C virus can trigger autoimmune thyroiditis by directly infecting thyroid cells; and identifying a novel small molecule that can block antigen presentation in autoimmune thyroiditis.

Current Projects

  1. 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.
  2. 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.
  3. ER stress and autoimmunity
    ER stress is emerging as an important link between environmental triggers, such as viral infections, and autoimmune thyroiditis and diabetes. Current studies are dissecting the mechanisms by which ER stress can trigger autoimmune thyroiditis and type 1 diabetes.
  4. Translational studies in autoimmune thyroiditis 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. 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.
  5. Genetic analysis 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 including CTLA-4, FOXP3, and GPR103. The group is now analyzing the mechanisms by which these genes predispose to disease. 
  6. The role of environmental factors in triggering autoimmune thyroiditis and type 1 diabetes
    Certain infections, specifically hepatitis C, are associated with autoimmune thyroiditis and diabetes. In addition, interferon alpha therapy for hepatitis C can also trigger autoimmune thyroiditis and diabetes. The Tomer lab showed that the hepatitis C virus can infect human thyroid cells in culture, demonstrating a direct effect of the virus on triggering thyroid autoimmunity. Current studies are aimed at dissecting the mechanisms by which hepatitis C virus and interferon alpha can trigger autoimmune thyroiditis and diabetes in genetically susceptible individuals.
  7. Environmental triggers of type 1 diabetes
    The frequency of type 1 diabetes has increased dramatically since WWII. The Tomer lab is screening environmental chemical exposures that may trigger type 1 diabetes and explain this rise in its incidence.

Selected Publications

  1. Li CW, Menconi F, Osman R, Mezei M, Jacobson EM, Concepcion E, David CS, Kastrinsky DB, Ohlmeyer M, Tomer Y. Identifying a small molecule blocking antigen presentation in autoimmune thyroiditis. The Journal of biological chemistry 2015 Dec;.
  2. Lipner EM, Tomer Y, Noble JA, Monti MC, Lonsdale JT, Corso B, Greenberg DA. Linkage Analysis of Genomic Regions Contributing to the Expression of Type 1 Diabetes Microvascular Complications and Interaction with HLA. Journal of diabetes research 2015 Oct; 2015.
  3. Hammerstad SS, Grock SF, Lee HJ, Hasham A, Sundaram N, Tomer Y. Diabetes and Hepatitis C: A Two-Way Association. Frontiers in endocrinology 2015 Sep; 6.
  4. Lee HJ, Li CW, Hammerstad SS, Stefan M, Tomer Y. Immunogenetics of autoimmune thyroid diseases: A comprehensive review. Journal of autoimmunity 2015 Jul;.
  5. Tomer Y, Dolan LM, Kahaly G, Divers J, D'Agostino RB, Imperatore G, Dabelea D, Marcovina S, Black MH, Pihoker C, Hasham A, Hammerstad SS, Greenberg DA, Lotay V, Zhang W, Monti MC, Matheis N. Genome wide identification of new genes and pathways in patients with both autoimmune thyroiditis and type 1 diabetes. Journal of autoimmunity 2015 Apr;.
  6. Li CW, Concepcion E, Tomer Y. Dissecting the role of the foxp3 gene in the joint genetic susceptibility to autoimmune thyroiditis and diabetes: A genetic and functional analysis. Gene 2014 Dec;.
  7. Lombardi A, Barlow Inabnet W, Owen R, Ellen Farenholtz K, Tomer Y. Endoplasmic reticulum stress as a novel mechanism in amiodarone-induced destructive thyroiditis. The Journal of clinical endocrinology and metabolism 2014 Oct;.
  8. Stefan M, Wei C, Lombardi A, Li CW, Concepcion ES, Inabnet WB, Owen R, Zhang W, Tomer Y. Genetic-epigenetic dysregulation of thymic TSH receptor gene expression triggers thyroid autoimmunity. Proceedings of the National Academy of Sciences of the United States of America 2014 Aug; 111(34): 12562-12567.
  9. Employing a recombinant HLA-DR3 expression system to dissect MCH II-thyroglobulin peptide dynamism: A genetic, biochemical, and reverse immunolgical perspective. J Biol Chem 2009; 284: 34231-34243.
  10. Tomer Y, Huber A. The etiology of autoimmune thyroid disease: A story of genes and environment. J Autoimm 2009; 32: 231-239.
  11. Villano MJ, Huber AK, Greenberg DA, Golden BK, Concepcion E, Tomer Y. Autoimmune thyroiditis and diabetes: Dissecting the joint genetic susceptibility in a large cohort of multiplex families. J Clin Endocrinol Metab 2009; 94: 1458-1466.
  12. Akeno N, Blackard JT, Tomer Y. HCV E2 protein binds directly to thyroid cells and induces IL-8 production: A new mechanism for HCV induced thyroid autoimmunity. J Autoimmun 2008; 31: 339-344.
  13. Huber A, Menconi F, Corathers S, Jacobson EM, Tomer Y. Joint genetic susceptibility to type 1 diabetes and autoimmune thyroiditis; From epidemiology to mechanisms. Endocr Rev 2008; 29: 697-725.
  14. Ban Y, Greenberg DA, Davies TF, Jacobson E, Concepcion E, Tomer Y. Linkage analysis of thyroid antibody production: Evidence for shared susceptibility to clinical autoimmune thyroid disease. J Clin Endocrinol Metab 2008; 93: 3589-3596.
  15. Menconi F, Monti MC, Greenberg DA, Oashi T, Osman R, Davies TF, Ban Y, Jacobson EM, Concepcion ES, Li CW, Tomer Y. Molecular amino acid signatures in the MHC class II peptide binding pocket predispose to autoimmune thyroiditis in humans and in mice.. Proc Natl Acad Sci USA 2008; 105: 14034-14039.

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