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Chris Hampe received her PhD at the Weizmann Institute of Science in Israel in 1997. She did her post-doctoral training in Dr. Åke Lernmark’s laboratory at the University of Washington, Seattle and is currently a Research Associate Professor at the Diabetes and Obesity Center of Excellence at the University of Washington.

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Research Interests

Dr. Hampe’s research interests center on human autoimmune diseases and the role of autoantibodies in disease pathogenesis with particular interest in Type 1 diabetes and Stiff Person Syndrome. More specifically, areas of focus are as follows.

The role of autoantibodies to GAD65 (GAD65Ab) in the pathogenesis of type 1 diabetes.

In marked contrast to the traditional view, our recent studies and preliminary results suggest that GAD65Ab are common in healthy individuals, but masked by epitope-specific anti-idiotypic antibodies.

Isolation and characterization of b96.11-specific B lymphocytes from human periperhal blood.

In collaboration with Dr. BenHar in Israel, we cloned and expressed five human monoclonal anti-idiptypic antibodies that bind specifically to b96.11. The antibodies will be used to specifically deplete b96.11-specific lymphocytes to interfere with the autoimmune pathogenesis leading to development of T1D.

Specific depletion of GAD65-specific B lymphocytes in NOD mice.

Injection with GAD65Ab-specific anti-Id-8E6G4 reduced the number of GAD65-specific B plasma cells by 85%. Investigation of GAD65-specific T cell responses in NOD mice injected with the above antibody are currently underway in collaboration with Dr. John Gebe, BRI.

GAD65Ab in Stiff Person Syndrome

GAD65Ab may have a pathogenic role in the disease process in patients with Stiff Person Syndrome (SPS). GAD65Ab in SPS patients inhibit the enzyme’s activity and result in a deficit in the major inhibitory neurotransmitter GABA, possibly causing clinical symptoms such as muscle spasms and stiffness. Often, the diagnosis of SPS is delayed due to its relative rareness and patients experience dilapidating clinical symptoms. Muscle stiffness and pain are common complaints in the general population. Often no physical cause can be found and appropriate treatment cannot be recommended. We hypothesize that autoimmunity to GAD65 is present in a sizeable portion of these cases.

In vivo administration of GAD65Ab into rat cerebellum

In collaboration with Drs. Honnorat and Manto in France and Belgium, we established that GAD65Ab play an active role in the pathogenesis of SPS. Such a role had been hypothesized based on the observation that SPS patients have high GAD65Ab titers which inhibit GAD65 enzyme activity and show decreased GABA concentrations. The mechanism of this pathogenesis remained however unclear. We continued our collaboration and investigation of the potential role of GAD65Ab in SPS. We found that GAD65Ab are internalized into a rat neuronal cell line. GAD65Ab injections induced behavioral changes in rats.

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How can this research help people with diabetes?

In our laboratory we carry out basic and clinical research to understand the etiology and pathogenesis of Type 1 Diabetes with the ultimate goal to develop a preventative treatment or cure for the disease.