5 Questions for a Researcher in Autoantibodies and Type 1 Diabetes

Amy Bevan–GluMomGluDanielleGluAmy; and Dr. Henry Anhalt

We sat down with Dr. Anette-Gabriele Ziegler, Chair of Diabetes and Gestational Diabetes at the Technische Universität München School of Medicine, to discuss her research on examining the risk between the presence of autoantibodies and the development of type 1 diabetes. (You can read about her work here.)

Are you suggesting screening be part of clinical pediatric care? How else would interested participants get screened?

Yes, this is the goal. Early diagnosis of type 1 diabetes may prevent diabetic ketoacidosis on a population level, reducing family burden and health care cost. It would also help to set new standards for early diagnosis of type 1 diabetes and education, and provide the opportunity to perform secondary prevention studies to prevent insulin dependence on a broad population based level and with rapid recruitment and outcome.

How does age correlate with the children who progressed from single to multiple islet autoantibodies? Are there further details on the progression from year to year?

The earlier islet autoantibodies appear, the faster the rate of disease progression. But on average, the rate is around 11% per year.

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Do you believe the rapid progression to multiple islet autoantibodies in the first two years of life is correlated to the immune system being compromised? If not, what do you believe is the reason for this short timeline?

We don’t really know, but I assume that islets are particularly susceptible to an immune attack in early life and that the immune system is more likely to produce cells which are ‘autoreactive’ during this time (autoreativity means that the immune cells are not only attacking foreign invaders but also—wrongly—the body’s own tissue).

In addition to examining the rapid progression to multiple islet autoantibodies, is there anything that can be done to further study and understand the development of diabetes in children?

Environmental exposures as well as metabolic conditions may also influence progression rates. Complex ‘omics’ technologies (metabolomics, proteomics, epigenomics) are applied to identify and understand the complex pathways which lead to type 1 diabetes. Such technologies are, for example, applied to blood samples collected from infants and children participating in the longitudinal TEDDY study.

What is known about those children who don’t progress quickly, or those with multiple autoantibodies who don’t develop clinical diabetes? How is age connected to the development of multiple autoantibodies in adults?

The majority if not all children with multiple islet autoantibodies will develop clinical diabetes, but in a few children this process will take more than one or two decades. Genetic non-HLA susceptibility markers may contribute to the rate of disease progression but altogether there is still little known about what protects children from progressing quickly. Multiple islet autoantibodies are less frequent in adults and LADA patients.




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