BU researchers test a new hypothesis to explain the cause of autoimmunity in patients with type 1 diabetes

Type 1 diabetes (T1D) is an autoimmune disease in which the pancreas produces little or no insulin. Details of the events that occur during autoimmune destruction of pancreatic beta cells have been widely studied, but the mystery of what causes autoimmunity is unknown. In a new study, researchers from Boston University School of Medicine (BUSM), Indiana University School of Medicine and Temple University School of Medicine present a testable hypothesis to explain the initiation of autoimmunity. If validated, this would allow early detection and possible prevention of T1D in susceptible people.

“Previous studies have focused on the triggers, genes, and proteins that differentiate individuals with T1D from those without diabetes, with an emphasis on the b cell (b cells create antibodies) as as the target of immune destruction and blood sugar as the primary abnormality. We focus on metabolic communication as an early initiator with the b cell as an active participant with immune cells,” explains corresponding author Barbara Corkey, PhD, Emeritus Professor of Medicine and Biochemistry at BUSM.

According to Corkey, her research led her to generate the testable hypothesis that the induction of autoimmunity is the consequence of one or more major inflammatory events in individuals with sensitive human leukocyte antigens (molecule present at the surface of most body cells that play an important role in the body’s immune response to foreign substances) phenotypes higher sensitivity to cytokines (substances secreted by certain cells of the immune system) and free fatty acids (FFA ).

“Diseases or environmental agents that dramatically increase cytokine production and/or elevate FFAs initiate autoimmune destruction in individuals with specific genetic characteristics. Thus, early prevention should aim to decrease elevated lipids and decrease the simultaneous excessive elevation of cytokines or cytokine and lipid-induced immune cell proliferation,” she adds.

Corkey thinks the characteristics that make individuals susceptible to autoimmune destruction could also apply to other autoimmune diseases such as toxic shock syndrome and possibly long COVID.

These results are published online in the journal Diabetes.


Boston University School of Medicine

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