"Type 1 diabetes is particularly tragic because it usually starts in childhood and its effects worsen with time. It can lead to organ damage, blindness and other terrible side effects.  That's why I focus so heavily on this disease.  I'm trained as a physician and I saw what it can do." - Matthias von Herrath, M.D.

Dr. von Herrath serves as Director of the Center for Type 1 Diabetes Research in addition to being a full Professor in the Division of Developmental Immunology. Dr. von Herrath's research focuses on strategies to prevent type 1 diabetes through the induction of regulatory T cells.

Dr. von Herrath wrote his thesis in the field of Biochemistry and then received his M.D. in Medicine from the Freiburg Medical School in Freiburg, Germany in 1988. He did his residency work at the Freiburg Medical Center in the Internal Medicine/Immunology department and at the Diakonic Hospital's Intensive Care Unit in Freiburg. For his postdoctoral work, Dr. von Herrath went to The Scripps Research Institute and worked in its Neuropharmacology and Immunology departments.

Dr. von Herrath is an editor and reviewer for numerous publications as well as being a member of the American Society of Clinical Investigation and a Council Member for the International Diabetes Society. In addition, he is an Adjunct Professor of Pediatrics at the University of California, San Diego. He is the recipient of the 2008 American Diabetes Association-Lilly Outstanding Scientist Achievement Award, the 2006 Grotzky Award from the Juvenile Diabetes Foundation International, and the 2007-2012 Scholar Award from the Juvenile Diabetes Foundation.

Matthias von Herrath, M.D., and his team study why the immune system sometimes attacks the body's own cells. They focus on type 1 diabetes, a disease caused by the immune system attacking the insulin-producing beta cells in the pancreas, and on diseases caused by viral infections. Their goal is to develop and evaluate new treatments and therapies for these conditions, in particular immune-based interventions.

The laboratory has found that stimulating the immune system with beta cell proteins via DNA vaccines results in a beneficial, or regulatory, immune response that can prevent type 1 diabetes. The DNA vaccines are currently being developed for the clinic in collaboration with BayHill therapeutics.

In addition, Dr. von Herrath's team is studying how introducing immune response modifiers, such as small molecules named "cytokines" or certain antibodies, get the immune system back on track, stopping it from attacking the body's own cells. His laboratory is collaborating with a major diabetes consortium in the United States and Australia, supported in part by the Juvenile Diabetes Foundation and the Medical Research Council in Australia, on developing this strategy. This approach has proved effective in animals in an advanced stage of type 1 diabetes, and the hope is that this will translate to human patients.

Viral infections and the diseases they cause can be modulated through similar pathways. In parallel to the approach followed by the laboratory for type 1 diabetes, the focus is on developing treatments that will be effective after the infection has occurred.

To read more about Dr. von Herrath's work visit the Type 1 Diabetes Center.

How viral infections enhance or prevent type 1 diabetes-from mouse to man. J Med Virol. 2011

Development of Autoimmune Diabetes in the Absence of Detectable IL-17A in a CD8-Driven Virally Induced Model. J Immunol. 2011

How does type 1 diabetes develop?: the notion of homicide or β-cell suicide revisited.
Diabetes. 2011

Nasal cardiac myosin peptide treatment and OX40 blockade protect mice from acute and chronic virally-induced myocarditis. J Autoimmun. 2011

TLR2 signaling improves immunoregulation to prevent type 1 diabetes. Eur J Immunol. 2011

Viral infection prevents diabetes by inducing regulatory T cells through NKT cell-plasmacytoid dendritic cell interplay. J Exp Med. 2011

Type 1 diabetes: etiology, immunology, and therapeutic strategies. Physiol Rev. 2011

Increased memory conversion of naïve CD8 T cells activated during late phases of acute virus infection due to decreased cumulative antigen exposure. PLoS One. 2011

A novel technique for the in vivo imaging of autoimmune diabetes development in the pancreas by two-photon microscopy. PLoS One. 2010

Humanizing animal models: a key to autoimmune diabetes treatment.
Sci Transl Med. 2011

Pathology and pathogenesis of virus infections. The Immune Response to Infection. 2011

Antigen-specific immunotherapy for type 1 diabetes: maximizing the potential. Diabetes. 2010

Combination therapies for type 1 diabetes: why not now? Immunotherapy. 2010

Immunotherapy of type 1 diabetes--how to rationally prioritize combination therapies in T1D. Int Immunopharmacol. 2010

Subcutaneous insulin B:9-23/IFA immunisation induces Tregs that control late-stage prediabetes in NOD mice through IL-10 and IFNgamma. Diabetologia. 2010

99th Dahlem conference on infection, inflammation and chronic inflammatory disorders: viruses, autoimmunity and immunoregulation. Clin Exp Immunol. 2010

Minimal effect of CD103 expression on the control of a chronic antiviral immune response.
Viral Immunol. 2010

Pre-existing autoimmunity determines type 1 diabetes outcome after Flt3-ligand treatment.
J Autoimmun. 2010

Essential role for TLR9 in prime but not prime-boost plasmid DNA vaccination to activate dendritic cells and protect from lethal viral infection. J Immunol. 2010

Viral triggers for autoimmunity: is the 'glass of molecular mimicry' half full or half empty?
J Autoimmun. 2010

Genetic-induced variations in the GAD65 T-cell repertoire governs efficacy of anti-CD3/GAD65 combination therapy in new-onset type 1 diabetes. Mol Ther. 2010

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