Researchers at Stanford University School of Medicine, Yale University School of Medicine, and the Hospital for Special Surgery Research Institute have uncovered new details about how the immune system prevents the production of antibodies that can recognize and damage the body's own, healthy tissues.
B cells are a type of white blood cell that help to fight off infections by producing antibodies capable of recognizing foreign molecules, known as antigens, produced by invading pathogens such as bacteria and viruses. But some B cells generate antibodies that recognize"self-antigens" produced by the body's own cells, potentially causing the immune system to attack healthy tissues by mistake, leading to a variety of autoimmune diseases.
The researchers discovered that depleting TLR9 impairs central tolerance and causes mice to produce increased numbers of self-reactive B cells and antibodies. Meffre and Barrat's teams found that TLR9 activity is also reduced in the B cells of patients with systemic sclerosis, an autoimmune disease that damages the skin, joints, and internal organs.
"Our data challenge the current paradigm that BCR signaling alone is responsible for the deletion of self-reactive B cells in the , since we demonstrate that TLR9 signaling plays an essential role in the establishment of central B cell tolerance," says Meffre, who is now a professor at Stanford University School of Medicine.and perhaps other autoimmune diseases, potentially by neutralizing CXCL4, may represent a novel therapeutic strategy to restore B cell tolerance.
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