Helena Reijonen

Helena Reijonen, Ph.D.

  • Associate Professor, Department of Diabetes Immunology

Helena Reijonen, Ph.D.

Research Focus :
  • Autoreactive T cells in type 1 diabetes
  • Monitoring of T cell responses in disease
  • Mechanisms of autoimmunity
Other Languages Spoken
  • Finnish
  • Swedish
Helena Reijonen, Ph.D., is an associate professor in the Department of Diabetes Immunology within the Diabetes & Metabolism Research Institute.

Reijonen came to the City of Hope from the Benaroya Research Institute in Seattle. Reijonen received her Ph.D. in the Immunogenetics Program at the University of Turku in Finland. She did her postdoctoral training at Benaroya Research Institute and started her own research group at the same institute in 2005. Her research focuses on the immunological pathways and functional mechanisms of autoimmunity and type 1 diabetes. 
  • 2016-present, Associate Professor, Diabetes Immunology, Diabetes & Metabolism Research Institute, City of Hope, Duarte, CA
  • 2005-2016, Research Assistant Member, Diabetes, Benaroya Research Institute, Seattle, WA
  • 2005-11, Affiliate Assistant Professor, Department of Immunology, University of Washington, Seattle, WA


  • 1994, Ph.D., Ilonen laboratory, Immunogenetics, Department of Microbiology, University of Oulu and University of Turku, Finland


  • 1989-1994, Ilonen laboratory, Immunogenetics, Department of Microbiology, University of Oulu and University of Turku, Finland
  • 1995-1999, Nepom Laboratory (Gerald Nepom, M.D., PH.D.), Virginia Mason Research Center, Benaroya Research Institute, Seattle, WA
Our research projects aim at understanding the characteristics of the immune cell repertoire, which is responsible for the destruction of insulin-producing beta cells, and how to regulate this process.
The focus of our research is  identification of the T lymphocytes relevant for the progression of type 1 diabetes and determining the phenotypic signature of these cells. We investigate autoantigen specific T cell responses in the individuals who are at risk but have not progressed to type 1 diabetes yet and in recent onset type 1 diabetes patients. In the subjects participating in the clinical trials, we study changes in the immune repertoire induced by targeted therapies. We also aim to discover new relevant determinants from the different islet cell proteins, novel phenotypic markers and pathways in autoimmunity, which will improve the sensitivity of disease prediction, monitoring and response to therapy. Furthermore, our interest is to gain deeper insight of the disease mechanisms mediated by genetic determinants associated with disease risk and protection.

Another important area of our research includes strategies to understand the pathways leading to the recurrence of autoimmunity and destruction of the transplanted pancreas or pancreatic islets in recipients with type 1 diabetes. Methodological advances such as tetramer-based assays offer an unprecedented opportunity to characterize specificity and the functional status of autoreactive T lymphocytes in the blood and in the biopsy tissues when available. These studies will provide critical information about the immunological mechanisms regulating recurrence of autoimmunity and islet destruction in the transplant patients.
Understanding the natural history of type 1 diabetes and staging the disease process requires expertise from many investigators at City of Hope. There is much needed knowledge on beta cell biology and inflammation which have been shown to modulate the micro environment in the pancreas, T cell profiling and modulatory effect of dendritic cells on the T cell response. Our new team in the Department of Diabetes Immunology has expertise in the post-translational modifications of islet autoantigens and examining the role of beta cell stress in the generation of de novo epitopes that can break the tolerance. City of Hope also has widely recognized excellence in beta cell transplantation, as well as strong core facilities including of bioinformatics and deep-sequencing, which allows in-depth profiling of the cells of interest. All these components are essential in the assembly of the complex picture of the mechanistic pathways playing a role in the pathogenesis of type 1 diabetes.
  • Ability to screen for the risk to develop type 1 diabetes and to stage autoimmune process from the first signs of autoimmunity (pre-diabetes) to insulin dependence is important for understanding the natural history of the disease. Understanding the diversity of underlying mechanisms of type 1 diabetes is critical for the need to design individualized therapy approach in the clinical intervention. We are using advanced immunological assays to study the low frequency autoantigen specific CD4 and CD8 T cells. We determine their specificity, phenotypic and gene expression profiles and the functional properties. We expect to discover novel biomarkers and pathways relevant for disease progression which will help us to understand the critical checkpoints in the pathogenesis of type 1 diabetes. Furthermore, understanding the diversity of the immune profile in those who develop type 1 diabetes is important for the stratification of the patients and selection of the appropriate therapeutic approach to intervene the disease progression.
  • Modern tools of monitoring the changes in antigen specific T cell repertoire in response to treatment in the clinical trials is a shared long-term interest between researchers at City of Hope. Informative markers, such islet autoantigen specific T cells with disease associated phenotype or the genetic variants, could also contribute to the understanding of mechanistic outcomes of the therapy by relating the observed clinical response to cellular or molecular pathways. Only by confirming these links we can identify causative immune phenotypes in type 1 diabetes, which could become the legitimate targets of drug development. In our studies, we analyze the functional phenotype of newly emerging T cells post-therapy, specifically, whether they recognize pre-existing or new targets and whether the immune profile has changed. It will be important to establish whether the post-immunization response is a result of mobilization and/or clonal expansion of existing autoreactive T cell clonotypes or engagement of naive cells with a different functional phenotype. It is also of ultimate importance to examine why some subjects are different and remain nonresponders to the treatment or are “outliers”. These studies could provide an entirely new perspective on autoimmune disease. We will explore whether there are many available T cells capable of responding to the autoantigen, and why the expansion of these repertoires is not a component of the natural history of the disease.
  • One of the most interesting questions in type 1 diabetes etiology is why some gene variants protect from the disease. We are investigating how genetic protection involves peripheral immune regulatory pathways. We expect to discover a regulatory phenotype in healthy individuals, or distinct features retaining differentiation to pathogenic functions. These studies will provide us with a greater insight into the basic understanding of T cell responses in autoimmunity and how they are regulated.
  • Our studies on the pancreas and islet transplantation recipients show that recurrence of autoimmunity is possible despite immunosuppression that prevents rejection. The samples collected from the long-term type 1 diabetes patients over time demonstrated persistent memory islet autoantigen specific T cell response. Long-lasting autoreactive memory is an obstacle for the goal of lasting insulin independency in the transplant setting. It can also be the reason why many immunomodulatory therapies fail to have long-lasting effect in recent onset type 1 diabetes, even when initially successful in maintaining the residual beta cell function. Our study will elucidate the importance of understanding the phenotypic profile of the islet autoreactive T cells before the transplantation at “baseline” and how it affects the outcome.
Daniel Zwick
Postdoctoral Fellow
Victoria King
Research Associate I
Carmen Fotino, Ph.D.
Staff Scientist
  • 2012-2016 Diabetes Research Center, University of Washington (affiliate member)
  • 2008-2016 Institute of Translational Health Sciences, WA (investigator)
  • 2006-present, Network for Pancreatic Organ Donors with Diabetes (member and investigator)
  • 2004-2013, NIH/NIDDK TrialNet (investigator, member, mechanistic outcomes committee, ad hoc reviewer)
  • 2003-present, Federation of Clinical Immunology Societies
  • 2000-2010, American Diabetes Association
  • 1995-present, Immunology of Diabetes Society
  • 2000, JDRF Career Development Award, Early career award
  • 1997, The Academy of Finland Medical Council postdoctoral fellowship award
  • 1995, The Academy of Finland Medical Council postdoctoral fellowship award
  • 1994, Paulo Foundation Award, Young investigator award
  • 1993, Novo Nordisk Foundation Award, Ph.D. student fellowship
  • 1993, Wihuri Foundation Award, Young investigator award
  • 1992, Alma and K.A. Snellman Foundation Award, Ph.D. student fellowship
  • 1992, Nordisk Insulin Fond Award, Ph.D. student fellowship
  • 1992, Zonta International Foundation Award, Young female investigator award
  • 1991, University of Oulu graduate student scholarship
  • 1990, Finnish Academy of Science graduate student fellowship
  • 1989, Alma and K.A. Snellman Foundation Award, Ph.D. student fellowship
  • 1989, Finnish Diabetes Foundation fellowship, Ph.D. student fellowship
  • 1988, Aaltonen Foundation fellowship, Ph.D. student fellowship
  • 1988, Alma and K.A. Snellman Foundation Award, Ph.D. student fellowship
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