Systemic lupus erythematosus (SLE) is an autoimmune disease where the immune system attacks the body´s own cells, causing a range of symptoms. A group of researchers found a genetic mutation in the UNC93B1 gene in young children with SLE, leading to overactivation of TLR7 and uncontrolled production of interferons, triggering an immune attack on normal cells. People lacking functional UNC93B1 are prone to viral infections. The findings are relevant for the development of targeted therapies for patients with SLE, indicating that blocking overactive TLR7 might be therapeutically effective. The study was funded by the German Research Foundation and the German Federal Ministry of Education and Research. The results were published in Science Immunology on January 11, 2024.

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