The autoimmune destruction of the pancreatic beta-cells in type 1 diabetes (T1D) has been studied extensively, yet the mystery of what causes autoimmunity is unknown. In a new study, researchers present a testable hypothesis to explain the initiation of autoimmunity – which, if validated, this would allow early detection and possible prevention of T1D in susceptible individuals. This hypothesis is discussed in the journal Diabetes.
“Previous studies have focused on the triggers, genes and proteins that differentiate individuals with T1D from those without diabetes with a focus on the b-cell (b-cells create antibodies) as a target of immune destruction and blood glucose as the main abnormality. Our focus is on metabolic communication as an early instigator with the b-cell as an active participant together with the immune cells,” explained corresponding author Barbara Corkey, PhD, professor at Boston University School of Medicine.
Prof Corkey’s research led her to hypothesise that autoimmunity induction results from one or more major inflammatory events in individuals with susceptible human leukocyte antigens phenotypes plus elevated sensitivity to cytokines and free fatty acids (FFA).
“Illnesses or environmental agents that dramatically increase cytokine production and/or elevate FFA initiate autoimmune destruction in individuals with specific genetic features. Thus, early prevention should be aimed at decreasing elevated lipids and diminishing excessive simultaneous elevation of cytokines or cytokine- and lipid-induced immune cell proliferation,” she said.
Prof Corkey believes that 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.
