Coaching the immune system to delay type 1 diabetes

In type 1 diabetes, the body does not produce insulin. Without this hormone, cells cannot use sugar in the bloodstream to fuel their activities. In the United States alone, according to the American Diabetes Association, type 1 diabetes affects approximately 1.3 million children and adults.

Experimental evidence supports a role for the immune system in the development of type 1 diabetes. While some components of the immune system promote the condition, it seems that others can help prevent it.

At Baylor College of Medicine, the laboratory of Dr. Massimo Pietropaolo has been studying type 1 diabetes for many years. One of his goals is to better understand how a branch of the immune system, the B cells, contributes to the disease.

Dr. Massimo Pietropaolo

“Increasing experimental evidence supports an important role of B cells in the development of diabetes, both in animal models and in humans,” said Pietropaolo, professor of medicine-endocrinology and McNair scholar at Baylor College of Medicine. “It’s been shown, for example, that subsets of immune B cells can directly contribute to disease development.”

However, there are also indications that subsets of B cells may be involved in modulating the onset of the condition, Pietropaolo explains. “For instance, elimination of a specific subset of B cells carrying the μ-chain marker resulted in impaired diabetes progression in a mouse model.”

In this study, Pietropaolo and his colleagues studied in more detail a specific subset of B cells, called CD19+ IgM+ B cells, and how they affected the onset of diabetes in a mouse model of the condition.

The researchers discovered that when they transferred CD19+ IgM+ B cells to mice, they delayed diabetes onset. The protective effect seems to be age specific. CD19+ IgM+ B cells from 6-week-old mice delayed diabetes onset, unlike CD19+ IgM+ B cells from mice older than 15 weeks.

We are the firsts to describe that CD19+ IgM+ B cells play a strong regulatory effect that delays diabetes onset in a mouse model,” Pietropaolo said.

“Taken together, our results open the future possibility of developing new therapies for this disease by expanding this specific B cell subtype pharmacologically and in turn modulating their regulatory actions in ways that would interfere with the onset of type 1 diabetes.”

Interested in reading all the details of his study? Find them in the journal JCI Insight.

Other authors of this work include Andrew D. Vonberg, María Acevedo-Calado, Aaron R. Cox, Susan L. Pietropaolo and Roberto Gianani, all from Baylor, and Steven K. Lundy from the University of Michigan Medical School.

This work was supported by McNair Medical Institute at The Robert and Janice McNair Foundation, NIH T32 Training grant (T32AI007413) and the Michigan Diabetes Research Training Center (MDRTC) funded by NIH grant 5P60-DK020572.

 

By Ana María Rodríguez, Ph.D.

 

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