Today in JCI Insight, researchers report that a subset of immune B cells can delay the onset of type 1 diabetes in mouse models. These findings open an opportunity to develop novel treatments for a subcategory of diabetes mellitus that affects about 420 million people around the world.
"For many years, one of the research interests of my lab has been to better understand the role the immune system plays in type 1 diabetes," says corresponding author Dr. Massimo Pietropaolo of Baylor College of Medicine.
Increasing experimental evidence supports that B cells, a subset of immune cells, play an important role in the development of diabetes—both in animal models and in humans. It's been shown, for example, that a certain type of B cell 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 the study, Pietropaolo and his colleagues looked in more detail at how a specific subset of B cells called CD19+ IgM+ B cells affect the onset of diabetes in a mouse model of the condition. The researchers discovered that when they transferred CD19+ IgM+ B cells to the mice, they were able to delay diabetes onset. The protective effect seemed to be age specific. CD19+ IgM+ B cells from 6-week-old mice delayed diabetes onset, but CD19+ IgM+ B cells from mice older than 15 weeks did not.
"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," says Pietropaolo.