Mice from a strain that ordinarily develops systemic lupus erythematosus (SLE), but bred with a deficiency in receptor for the protein Interleukin 21, stayed healthy and exhibited none of the symptoms of the disease, researchers at The Jackson Laboratory and National Institutes of Health report.
SLE is an autoimmune disease, with symptoms of varying severity including include painful or swollen joints, unexplained fever and extreme fatigue. An estimated 2 million Americans - 9 out of 10 of them female - live with SLE.
The primary job of the immune system is to identify and vanquish potentially dangerous infectious pathogens. Autoimmune diseases develop when immune system instead unleashes this potent defense system against the individual's own tissues, with predictably severe consequences.
Unlike other autoimmune diseases such as Type 1 diabetes, in which the immune response is focused on certain tissues, SLE is a systemic disease in which abnormal antibodies are produced that injure a variety of tissues and organs, including the skin, heart, lungs and kidneys.
The cause of SLE is not well understood, but recent work by a Jackson Laboratory research team led by Professor Derry Roopenian is shedding light on how the disease develops and offers hope for better therapies.