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...
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