Dr. Dai received his Ph.D. from the Memorial University of Newfoundland, Canada focusing on immunology. He served as a Research Fellow at the La Jolla Institute for Allergy & Immunlogy, San Diego from 2001-2002, and completed his postdoctoral training within TPIMS' Division of Immune Regulation in 2005. Dr. Dai is a Senior Research Scientist.

Research Focus

Dr. Dai's expertise is in the areas of autoimmunity, particularly in the prototypic T-cell-mediated autoimmune diseases, type I diabetes (T1D). An autoimmune response occurs following a triggering event, although in many autoimmune diseases such events are not defined. These triggering events are likely encountered quite frequently in any individual's lifetime, but autoimmune disease is still rare despite that there has been a measurable increase in recent years. From recent advances in the definition of genes causing autoimmune disease, it has been shown that the dysregulation of the normally well-balanced immune regulatory network is in large part attributable to combinations of common alleles of immune genes. These genes, along with environmental factors that can affect the regulatory network, can transform a homeostatic immune response, which includes self-specific T and B cells, into a pathological autoimmune disease.

Dr. Dai's long-term research efforts will focus on understanding the immune regulatory network by dissecting individual cellular and molecular components whose functions might be involved in the process of building this network. T-helper cells as a group are characterized by sensitive detection of antigens, rapid amplification after stimulation, readiness to differentiate to a variety of subsets and most importantly, a great diversity. It is these features of the T-helper cells that place them at the center of the immune system to provide the finest regulation, so as to maintain a healthy immune system that is ensured of effective immunity but purged of autoimmunity. By characterizing individual autoreactive T-helper cell clones including their fine antigen specificity, their antigen receptor sequence as well as their functional profiles following alterations of the known autoimmune-prone, genetic or environmental factors, identification of some of the essential cells, genes or pathways that are dysregulated in animals as well as in the human species may be made.

Honors and Awards

• Travel Award, American Association of Immunologists (AAI), Miami, USA, 2007.
• Postdoctoral Fellowship Award, Juvenile Diabetes Research Foundation, 2004-2006.
• Colman Graduate Student Award, outstanding Ph.D. student in the Faculty of Medicine, Memorial University of Newfoundland, Canada, 2002.
• First prize, Outstanding Academic Performance and Potential for Ph. D. students, Department of Immunology, Memorial University of Newfoundland, Canada, 2000.
• Second prize, Immunology Student Forum, Memorial University of Newfoundland, Canada, 1998.
• Graduate student fellowship, Memorial University of Newfoundland, Canada, 1996-2000.

1. Y. Dai, K. Carayanniotis, P. Eliades, P. Lymberi, P. Shepherd, Y-C. Kong and G. Carayanniotis. Enhancing or suppressive effects of antibodies on processing of a pathogenic T-cell epitope in thyroglobulin. J. Immunl. 1999, 162: 6987-6992.
2. Wang HY, Altman Y, Fang D, Elly C, Dai Y, Shao Y, Liu YC. Cbl Promotes Ubiquitination of the T Cell Receptor zeta through an Adaptor Function of Zap-70, J Biol Chem. 2001, 276:26004-11.
3. Y. D. Dai, V. P. Rao and G. Carayanniotis. Enhanced iodination of thyroglobulin facilitates processing and presentation of a cryptic pathogenic peptide J. Immunol. 2002,168:5907-5911.
4. Y. D. Dai, P. Eliades, K. A. Carayanniotis, D. J. McCormick, Y. M. Kong, P. Kordopatis, P. Lymberi and G. Carayanniotis. Thyroxine-binding Antibodies Inhibit T-cell Recognition of A Pathogenic Thyroglobulin Epitope. J. Immunol. 2005, 174(5):3105-10.
5. Y. D. Dai, K. P. Jensen, A. Lehuen, E. L. Masteller, J. A. Bluestone, D. B. Wilson, E. E. Sercarz. A Peptide of Glutamic Acid Decarboxylase 65 Can Recruit and Expand a Diabetogenic T cell Clone, BDC2.5, in the Pancreas, J. Immunol. 2005, 175:3621-3627.
6. Yang D. Dai, George Carayanniotis and Eli Sercarz. Spreading of autoimmunity via reciprocal activation of autoantigen-specific T and B cells. Cellular & Molecular Immunology, 2005, 2(3):169-175.
7. Y. D. Dai, K. P. Jensen, I. Marrero, N. Li, A. Quinn, and E. E. Sercarz. N-terminal flanking residues of a diabetes-associated GAD65 determinant are necessary for activation of antigen-specific T cells in diabetes-resistant mice. Eur. J. Immunol. 2008 (in press).
8. Y. D. Dai and E. E. Sercarz. Antigen processing patterns determine GAD65-specific regulation vs. pathogenesis. Frontiers in Bioscicence 2008 (in press).

1. Y. Dai. Mechanisms promoting the generation of cryptic T-cell epitopes in thyroglobulin. Center for Neurologic Diseases, Brigham and Women's Hospital in Harvard, Mar. 1999 (Invited talk).
2. Y. Dai and G. Carayanniotis, 2000, Thyroxine-specific antibodies block T-cell recognition of a pathogenic thyroglobulin epitope, the annual Meeting of Canadian Society for Immunology, Chateau-Bromont, QC, Canada (Oral presentation).
3. Y. D. Dai. Cbl, an E3 ligase, negatively regulates TCR signaling in thymocytes, and its deficiency results in enhanced central tolerance. Department of Pathology, Harvard Medical School, Dec. 2001 (Invited talk).
4. Y. D. Dai, K. Jensen, E. L. Masteller, J. A. Bluestone, D. B. Wilson, A. Lehuen, E. E. Sercarz. Glutamic acid decarboxylase (GAD) 65 regulates recruitment and expansion of a diabetogenic T cell clone, BDC2.5, in the pancreas. Keystone Symposium, Feb. 10-15, 2004 in Banff (Poster presentation).
5. Y.D. Dai, M. Stinson, N. Li, A. Quinn, E.E. Sercarz. Degradation and recycling of the T cell receptor mediates hyperresponsiveness of T cells in non-obese diabetes mouse. Clin. Invest. Med. 2004, 27, 4 p.162A, M38.6 (Abstract).
6. Y. D. Dai, and E. Sercarz. Genetic defect(s) mediates T cell hyperresponsiveness in NOD mouse by affecting the balance between degradation and recycling of T cell receptors following activation. 4th International Workshop on Antigen processing and Presentation, Sept 16-19, 2004 in Bar Harbor, USA (Poster presentation).
7. Y. D. Dai and E. E. Sercarz et al. Processing and presentation of GAD65 peptides determines the pathogenic and regulatory activity of a diabetes-related T cell clone, BDC2.5, Experimental Biology—AAI, Mar. 31 — Apr. 5, 2005 in San Diego (Oral presentation).
8. Y. D. Dai, I. Marrero, K. P. Jensen, N. Li, A. Quinn and E. Sercarz. Highly focused pathogenic response to a GAD65 peptide in NOD but not NOR mice can be attributed to vigorous processing of the flanking peptide residues. Keystone Symposia: Tolerance, Autoimmunity and Immune Regulation, Mar. 21 - 26, 2006, Breckenridge, Colorado (Poster presentation).
9. I. G. Marrero, Y. D. Dai, and E. E. Sercarz. Cyclophosphomide treatment of the NOD mouse reveals quasi-public dominant T cell clones. The 94th Annual Meeting of the American Association of Immunologists (AAI), May 18-22, 2007 in Miami (Poster presentation).
10. Y. D. Dai, B. Shirdel, S. Chau, P. Gros, L. S. Wicker and E. E. Sercarz. Nramp1 enhances autoimmune diabetogenic T cell response by altering the processing and presentation of pancreatic islet antigens in dendritic cells. The 7th Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS), June 7-11, 2007 in San Diego (Poster presentation).
11. I. G. Marrero, Y. D. Dai, and E. E. Sercarz. Tracking putative pathogenic members of the T cell repertoire in NOD mice. The 7th Annual Meeting of the Federation of Clinical Immunology Societies (FOCIS), June 7-11, 2007 in San Diego (Poster presentation).
12. Y. D. Dai, B. Shirdel, P. Gros, L. Wicker and E. Sercarz. Nramp1-mediated processing and presentation of diabetes-associated T cell determinants. 5th International Workshop on Antigen processing and Presentation, Oct. 7-11, 2007 in Dunk Island, Australia (Oral presentation).
13. Y. D. Dai, I. Marrero, Y. Li, A. E. Rottero, K. Schroder, D. B. Wilson and E. E. Sercarz. Unique Processing and Presentation of a Region of Glutamic Acid Decarboxylase (GAD) 65 Is Required for Activation of a Diabetic T Cell Clone. The 95th Annual Meeting of the American Association of Immunologists (AAI), April 2008 in San Diego (Poster presentation).