Matthias von Herrath, M.D., is the Director and Professor for the Diabetes Center at La Jolla Institute of Allergy and Immunology and Adjunct Professor, Department of Pediatrics at the University of California, San Diego.
He received both his undergraduate degree in biochemistry and his graduate degree in immunology from Freiburg Medical School in Freiburg, Germany. He completed his residency at Duakonic Hospital in Freiburg.
Dr. von Herrath’s research focuses on improving understanding the regulation of autoimmune injury and anti-viral responses.
Combination therapies in recent-onset type 1 diabetes
Dr. von Herrath's goal is to pre-clinically test suitable combination therapies using short-term administrations of systemically acting immune modulators such as anti-CD3 or anti-CD20, which are currently in clinical trials, and combine them with approaches to achieve antigen-specific tolerance to beta cells. Among these are DNA vaccines first described by his team in 1999, mucosal tolerance using nasal or oral insulin, as well as peptide- or protein-based therapeutics (for example, collaborative work with Diamyd's GAD). The aim is to enhance efficacy and reduce undesirable systemic side effects from immunosuppression. The challenge is to control immune memory T-cells to islet antigens long-term.
Live imaging of islet destruction by 2-photon microscopy
Their goal here is to observe the entry and mode of action under live conditions of islet destructive autoreactive CD8 T-cells and study how they can be regulated once they have reached the pancreas in vivo. Dr. von Herrath has developed a technique that allows to image live islets under attack in vivo.
Viral infections and T1D
In collaboration with nPOD, Dr. von Herrath and his team have begun to systematically test whether signs of viral footprints such as MHC class i upregulation or interferon production, as well as antiviral CD8 cells, can be found in human islets of patients with type 1a diabetes. So far, their findings show autoreactive CD8 cells are present (in collaboration with Bart Roep) and that many islets exhibit high levels of class I without major signs of immune infiltration.
Viral infections and Tregs
Dr. von Herrath and his team wants to understand how virus infections influence the effector functions and trafficking of regulatory T-cells. Stability of natural and induced Tregs is important to understand for optimizing their therapeutic induction and use. Antigen-specific Treg therapy, in their opinion, constitutes the holy grail of immunotherapy for type 1 diabetes, because they can act locally in the pancreatic lymph node and islets almost like a site-specific drug delivery vehicle, thus circumventing systemic side effects, and because they can bystander suppressive multiple autoaggressive T-cell specificities, which appear to be present in patients with advanced T1D.
Cytokines in T1D
Their goal here is to understand which cytokines are regulatory and which cytokines are destructive for beta cells. Current efforts focus on Il-21, IL-17, IL-10, IL-4, TGF-beta and interferon gamma. Better understanding of how cytokines regulate T1D pathogenesis will enable Dr. von Herrath and his team to use them in a targeted way as biomarkers for aggressive and regulatory T-cells and thus improve therapeutic options for T1D.
Dr. von Herrath has been the recipient of the Juvenile Diabetes Foundation Career Development Award and the George Kohler Award from the German Society of Immunology. In 2008, he received the Lilly Outstanding Scientific Achievement Award from the American Diabetes Association.
“It is a privilege and honor to be part of the Brehm coalition, which is the most productive and cooperative scientific coalition that I have ever been part of. Many fruitful cooperations have already emerged from this and Bill Brehm’s seed funding has enabled many of us to rapidly embark on scientific journeys that would otherwise be considered too risky and early stage to be funded! I believe that our coalition will make a major impact on accelerating the path towards a cure of type 1 diabetes.”