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<\/p>\nType 1 diabetes (T1D) is an autoimmune disease in which the pancreas makes little or no insulin. The details on the events that occur during autoimmune destruction of the pancreatic beta-cells have been studied extensively yet the mystery of what causes autoimmunity is unknown. In a new study, researchers from BUSM, Indiana University School of Medicine and Temple University School of Medicine, present a testable hypothesis to explain the initiation of autoimmunity.\u00a0 If validated, this would allow early detection and possible prevention of T1D in susceptible individuals.<\/p>\n
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\u201cPrevious 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,\u201d explains corresponding author Barbara Corkey, PhD, professor emeritus of medicine and biochemistry at BUSM.<\/p>\n
According to Corkey, her research led her to generate the testable hypothesis that the induction of autoimmunity is a consequence of one or more major inflammatory events in individuals with susceptible human leukocyte antigens<\/span> (molecule found on the surface of most cells in the body that play an important part in the body’s immune response to foreign substances)<\/span> phenotypes plus elevated sensitivity to cytokines (substances secreted by certain cells of the immune system) and free fatty acids (FFA).<\/p>\n \u201cIllnesses 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,\u201d she adds.<\/p>\n 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.<\/p>\n