Type 1 diabetes (T1D) is an autoimmune disease in which the pancreas produces little or no insulin. The details of the events that occur during the autoimmune destruction of beta-cells in the pancreas have been extensively studied, but the mystery of the causes 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 initiation 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 creating antibodies) as a target for immune destruction and blood glucose as the main abnormality. Our focus is on metabolic communication as an early promoter of the B cell as a participant. Active with immune cells,” explains corresponding author Barbara Corky, PhD, emeritus professor of medicine and biochemistry at BUSM.
According to Corky, her research led her to create a testable hypothesis that autoimmune induction is the result of one or more major inflammatory events in individuals with sensitive human leukocyte antigens (a molecule found on the surface of most cells in the body that plays an important part in the response). The body’s immunity to foreign substances) phenotypes as well as an elevated sensitivity to cytokines (substances secreted by certain cells of the immune system) and free fatty acids (FFA).
“Diseases or environmental factors that significantly increase cytokine production and/or increase FFA begin to destroy autoimmunity in individuals with specific genetic traits. Thus, early prevention should aim to reduce elevated lipids and reduce simultaneous excessive elevation of cytokines or cytokines and lipids that caused by the proliferation of immune cells.
Corky believes that the properties that make individuals susceptible to autoimmune destruction could also apply to other autoimmune diseases such as toxic shock syndrome and possibly prolonged COVID.
These results appear online in the journal diabetic.