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Diabetes breakthrough

B cells linked to the promotion of insulin resistance

Potential therapeutic targets for type 2 diabetes

Researchers from Boston University School of Medicine have reported that B cells (white blood cells of the immune system) secrete pro-inflammatory ratio cytokine proteins, which promote the insulin resistance that characterises type 2 diabetes.

"Now that we have identified the specific mechanisms by which B cells promote inflammation, we can help develop novel, targeted approaches to treat type 2 diabetes," said Dr Barbara Nikolajczyk, associate professor of microbiology at Boston, and senior author of the study. "Our study supports the continued exploration of FDA-approved B cell depletion drugs, which are known to be generally safe and effective, as novel agents to prevent obesity-associated inflammation and type 2 diabetes."

Barbara Nikolajczyk

The study, published in the Proceedings of the National Academies of Sciences, also demonstrated that B cells directly regulate inflammatory T cells, an immune cell type known to cause insulin resistance in animal models of disease.

Previous research has shown that B cells promote inflammation and can lead to the development of type 2 diabetes, but the mechanisms underlying B cell function were unclear.

The outcomes of this study showed that B cells from obese mice produce a pro-inflammatory cytokine profile, compared with B cells from lean mice. Additional in vivo studies show that obese mice without B cells have decreased systemic inflammation, inflammatory B- and T-cell cytokines, adipose tissue inflammation and insulin resistance, compared with normal obese mice.

The reduced inflammation in these obese/insulin resistant mice was associate with an increase in anti-inflammatory regulatory T cells (Tregs). This increase contrasts with the sharply decreased percentage of Tregs in obese compared with lean normal mice.

The results show that B cells from type 2 diabetes (but not non- type 2 diabetes) subjects support pro-inflammatory T-cell function in obesity/ type 2 diabetes through contact-dependent mechanisms, claim the study authors.  In contrast, human monocytes increase pro-inflammatory T-cell cytokines in both type 2 diabetes and non- type 2 diabetes analyses.

“These data support the conclusion that B cells are critical regulators of inflammation in type 2 diabetes due to their direct ability to promote pro-inflammatory T-cell function and secrete a pro-inflammatory cytokine profile,” the researchers conclude. “Thus, B cells are potential therapeutic targets for type 2 diabetes.”

The research included in this study was supported in part by the National Institutes of Health's National Institute of Diabetes and Digestive and Kidney Diseases and the Boston Nutrition Obesity Research Center.

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