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The new findings could lead to better treatments for rheumatoid arthritis, lupus and other inflammatory diseases – and may even help us slow aging.

Researchers have discovered how “leaky” mitochondria can drive harmful inflammation responsible for diseases such as lupus and rheumatoid arthritis. Scientists may be able to leverage the findings to develop better treatments for those diseases, improve our ability to fight off viruses and even slow aging.

The new discovery reveals how genetic material can escape from our cellular batteries, known as mitochondria, and prompt the body to launch a damaging immune response...

Oxidized DNA (green) accumulates in the mitochondria (red) of neutrophils isolated from SLE patients.

Baylor Institute for Immunology Research has discovered the neutrophils of systemic lupus erythematosus (SLE) patients release oxidized DNA from their mitochondria that can stimulate an unwanted immune response. The study suggests that targeting the pathways that lead to the accumulation of this DNA and/or facilitate its removal could be new ways to treat this chronic autoimmune disease.

Though the initial trigger for SLE remains unknown, it is characterized by the generation of autoantibodies that recognize the patient’s own DNA or RNA-protein complexes and the excessive production of type I interferons, signaling proteins that activate the body’s immune response...