Published April 25, 2016
Arthritis & Rheumatology
Experts have known for some time that Type I interferon (IFN) plays a critical role in the progression of lupus nephritis (LN), a dangerous complication that affects as many as 60 percent of people with lupus at some point in their lives.
Now, a team of scientists from Cincinnati Children’s and several institutions in China has tracked down a specific microRNA that controls the IFN pathway in renal cells. Their findings appear in the April 2016 issue of Arthritis & Rheumatology.
Their analysis shows that microRNA-130b (miR-130b) is under-expressed in kidney tissues of patients and lupus-prone mice. This under-expression correlates with heightened abnormal activation of the IFN response in LN patients.
Overexpression of a synthetic mimic of miR-130b in mice reduced kidney damage. Testing found decreased proteinuria, lower levels of immune complex deposition, and lack of glomerular lesions.
“Showing that manipulating this novel disease pathway regulator is possible is an important first step toward developing new, potentially life-saving treatments for people with lupus,” says John Harley, MD, PhD, director of the Center for Autoimmune Genomics and Etiology (CAGE).
Currently, doctors use corticosteroids, immune-suppressing agents and other drugs to control LN. However, these drugs pose serious side-effect risks. A new option would be welcome because even with treatment, some patients develop kidney failure and require dialysis and/or a kidney transplant to survive.
To advance these findings, Harley and colleagues plan to evaluate this and other mimics and antagonists of miRNAs for their impact on the processes that lead to lupus and LN.