A chance discovery during research on mice has provided new insight into a cellular process that may be associated with increased risk for developing lupus. Researchers at St. Jude Children’s Research Hospital have discovered that defects in a process called LC3-associated phagocytosis (LAP) may provoke a lupus-like autoimmune disorder. LAP is essential to the digestion and disposal of dead and dying cells after they have been eaten by immune scavenger cells called macrophages. LAP additionally recruits components of another housekeeping system called autophagy to digest what the macrophages eat. In the current research, it was noted that LAP-deficient mice were smaller than mice without this defect. In addition they exhibited higher levels of inflammation, autoimmune antibodies, and other changes that are associated with systematic lupus erythematosus (SLE) in humans. The findings were published online earlier this week in Nature.
SLE, the most common form of lupus, affects some 322,000 patients in the US. It occurs when the immune system makes antibodies that target the patient’s tissue, causing widespread inflammation and damage to both tissue and organs. The research team tested their theory of association by injecting dying cells into LAP-deficient mice. They noted an increase in signs of lupus-like illness, including an increase in antibodies that attack normal tissue, in comparison to mice in which LAP functioned normally. Work is underway to identify LAP defects in humans and to explore its association to other inflammatory diseases.
Read a news story about the study findings here.
The journal article summary may be read here.