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Yang D. Dai

Yang D. DaiTorreyPinesInstituteCA

Assistant Member

858.597.3808 - phone
858.597.3804 - fax
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Dr. Dai’s laboratory uses T cell lines or clones to study how altered antigen processing and presentation contributes to the activation of autoreactive T cells. Using animal models for autoimmune thyroiditis and type 1 diabetes (T1D), Dr. Dai has investigated several aspects of antigen processing and presentation; these include studying the antigen delivery pathway following formation of immune complexes, the effects of post-translational modifications on antigen processing and creating neo-determinants, and the distinct features of B cells in antigen presentation. The underlying hypothesis for these studies is that some non-tolerant, cryptic, or modified T cell determinants of self antigens may be exposed to the immune system under stress or inflammatory situations, which may lead to autoimmune disease in genetically susceptible individuals.

Current research projects:

  1. Using animal models of juvenile T1D to study genetic factors that cause the autoimmune attack of the pancreatic, insulin-secreting beta cells. We focus on studying genes involved in the antigen processing machinery, particularly the Slc11a1 gene.
  2. Studying the beta-cell-specific autoreactive T cell clones, their antigens and receptor sequences, and functional profiles, to understand the intrinsic endogenous pathways that selectively activate highly autoreactive T cell clones.
  3. Studying innate and adaptive autoimmune responses to microparticles or exosomes. Exosomes are small microparticles (<100 nm) that are released by normal cells, and under abnormal conditions they can become pro-inflammatory.

An autoimmune response occurs following a triggering event, which could be an infectious pathogen such as virus, or a non-infectious agent such as superantigen, or an environmental factor such as iodine, or a physiological reaction to stress or cell death. For many autoimmune diseases, the triggering events are unknown or are too diverse to be identified. Nevertheless, many organ-specific autoimmune diseases can be induced in animal models by tissue-specific autoantigens or peptides delivered in adjuvant, or by transferring tissue-specific autoreactive lymphocytes, particularly T cells. Therefore, autoimmune responses might be initiated by triggering events that activate specific autoreactive T cells. It is likely that during our lifetimes we all encounter environmental triggers that can activate autoreactive T cells, but only small number of people unfortunately develop autoimmune disease. Even so, there has been a significant increase in the incidence of autoimmune disease in recent years. By studying the association between genes and disease, we have learned that dysfunctions in the immune regulatory network contribute the most to such disease. Within this network, T helper cells are central to the regulation required for a healthy immune system to ensure effective immunity while preventing autoimmunity. T helper cells are characterized by their sensitivity to antigens, rapid amplification after stimulation, readiness to differentiate to a variety of subsets and most importantly, a great diversity. Currently, many strategies are being developed to target this lymphocyte population to treat patients by rescuing the dysregulated immune system. Future efforts are aimed at understanding the factors or events that trigger the autoreactive T cells, and this work might yield new targets for disease prevention and treatment.


  • 2002, Ph.D. (Immunology), Memorial University of Newfoundland, St. John’s, Canada


  • 2008 – present, Assistant Member, Torrey Pines Institute for Molecular Studies
  • 2005 – 2008, Senior Research Scientist, Torrey Pines Institute for Molecular Studies
  • 2002 – 2005, Postdoctoral Fellow, Torrey Pines Institute for Molecular Studies
  • 2001 – 2002, Research Fellow, La Jolla Institute for Allergy & Immunology

Professional Affiliations

  • 2008 – present, The American Association of Immunologists (AAI)
  • 2009 – present, Clinical Immunology Society (CIS)

Honors and Awards

  • 2009, Travel award, The Juvenile Diabetes Research Foundation Intl. (JDRF).
  • 2009, Selected for an oral presentation in the annual FOCIS meeting in San Francisco.
  • 2008-2011, Mentored Research Scientist Development Award (K01), NIH/NIDDK, USA.
  • 2007, Travel Award, The American Association of Immunologists (AAI), Miami, USA.
  • 2004-2006, Postdoctoral Fellowship Award, JDRF.
  • 2000, Colman Graduate Student Award, Memorial University of Newfoundland, Canada.

Selected Publications (10 of 18)

  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. 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.
  3. 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.
  4. Y. D. Dai, K. P. Jensen, A. Lehuen, E. L. Masteller, J. A. Bluestone, D. B. Wilson and 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.
  5. Y. D. Dai, G. Carayanniotis and E. Sercarz. Spreading of autoimmunity via reciprocal activation of autoantigen-specific T and B cells. Cellular & Molecular Immunology, 2005, 2(3):169-175.
  6. F. R. He, H. F. Zhu, H. Huang, Y. D. Dai, X. Shen, M. Wang, L. Li, W. Xing and G. X. Shen. Programmed death-1 ligands-transfected dendritic cells loaded with glutamic acid decarboxylase 65 (GAD65) inhibit both the alloresponse and the GAD65-reactive lymphocyte response. Clin Exp Immunol. 2008, 151(1):86-93.
  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, 38(4):968-76.
  8. Y. D. Dai and E. E. Sercarz. Antigen processing patterns determine GAD65-specific regulation versus pathogenesis. Frontiers in Bioscience 2009 14, 344-351.
  9. Y. D. Dai, I. Marrero, P. Gros, H. Zaghouani, L. S. Wicker and E. E. Sercarz. Slc11a1 enhances the autoimmune diabetogenic T-cell response by altering processing and presentation of pancreatic islet antigens. Diabetes, 2009 58:156-164.
  10. Oligoclonality and innate-like features in the TCR repertoire of type II NKT cells reactive to a beta-linked self-glycolipid. P. Arrenberg, R. Halder, Y. Dai, I. Maricic and V. Kumar. Proc Natl Acad Sci U S A. 2010 Jun 15;107(24):10984-9. PMID: 20534460.