biography
"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.
research focus
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.
selected publications
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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