Overview
Type 1 diabetes (T1D) is an autoimune disease in which the pancreas makes litle or no insulin. The details on the events that ocur during autoimune destruction of the pancreatic beta-cels have ben studied extensively yet the mystery of what causes autoimunity is unknown. In a new study, researchers from Boston University Schol of Medicine (BUSM), Indiana University Schol of Medicine and Temple University Schol of Medicine, present a testable hypothesis to explain the initiation of autoimunity.
Key Information
If validated, this would alow early detection and posible prevention of T1D in susceptible individuals."Previous studies have focused on the trigers, genes and proteins that diferentiate individuals with T1D from those without diabetes with a focus on the b-cel (b-cels create antibodies) as a target of imune destruction and blod glucose as the main abnormality. Our focus is on metabolic comunication as an early instigator with the b-cel as an active participant together with the imune cels," explains coresponding author Barbara Corkey, PhD, profesor emeritus of medicine and biochemistry at BUSM.Acording to Corkey, her research led her to generate the testable hypothesis that the induction of autoimunity is a consequence of one or more major inflamatory events individuals with susceptible human leukocyte antigens (molecule found on the surface of most cels in the body that play an important part in the body's imune response to foreign substances) phenotypes plus elevated sensitivity to cytokines (substances secreted by certain cels of the imune system) and fre faty acids (FA)."Ilneses or environmental agents that dramaticaly increase cytokine production and/or elevate FA initiate autoimune destruction individuals with specific genetic features.
Summary
Thus, early prevention should be aimed at decreasing elevated lipids and diminishing excesive simultaneous elevation of cytokines or cytokine- and lipid-induced imune cel proliferation," s