Type 1 diabetes (T1D) is an autoimmune disease in which the pancreas produces little or no insulin. The details about the events that occur during autoimmune destruction of pancreatic beta cells have been extensively studied, but the mystery of the cause of 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 genesis of autoimmunity. If validated, this would allow early detection and potential prevention of T1D in susceptible individuals.
“Previous studies have focused on the triggers, genes and proteins that distinguish individuals with T1D from those without diabetes, with a focus on the b-cell (b-cells create antibodies) as the target of immune destruction and blood glucose as the main abnormality. focus is on metabolic communication as an early initiator with the b-cell as an active participant along with the immune cells,” explains corresponding author Barbara Corkey, PhD, professor emeritus of medicine and biochemistry at BUSM.
According to Corkey, her research led her to generate the testable hypothesis that the induction of autoimmunity is a result of one or more major inflammatory events in individuals with susceptible human leukocyte antigens (molecule found on the surface of most cells in the body that play an important role in role in the body’s immune response to foreign substances) phenotypes plus increased sensitivity to cytokines (substances secreted by certain cells of the immune system) and free fatty acids (FFA).
“Diseases or environmental factors that dramatically increase cytokine production and/or increase FFA cause autoimmune destruction in individuals with specific genetic characteristics. Thus, early prevention should focus on reducing elevated lipids and reducing excessive co-elevation of cytokines or cytokine- and lipid-induced proliferation of immune cells,” she adds.
Corkey believes that the characteristics that predispose individuals to autoimmune destruction could also apply to other autoimmune diseases, such as toxic shock syndrome and possibly prolonged COVID.
These findings appear online in the journal diabetes mellitus.
Boston University School of Medicine