Scientists from The Scripps Research Institute (TSRI) have identified a specific microRNA (miR-148a) that appears to be a key regulator of B-cell immune tolerance and that, when elevated, can be the cause of autoimmune diseases such as systemic lupus erythematosus (SLE or lupus). The scientists found that elevated levels of the small non-coding molecule miR-148a allow self-reactive immune B-cells to escape into the blood stream and attack the body’s own tissues. The research was published online on February 22, 2016, in the journal Nature Immunology. The article is titled “The microRNA miR-148a Functions As a Critical Regulator of B Cell Tolerance And Autoimmunity.” Alicia Gonzalez-Martin, first author of the new study, was excited by the discovery. “This is the first miRNA implicated in the regulation of B cell tolerance,” she said. “This is a good target for future therapies,” said TSRI Associate Professor Changchun Xiao, who was co-senior-author of the study with TSRI Professor David Nemazee. “We now know that this is causative—it’s not just a side effect.” Immune cells known as B-cells develop in the bone marrow and acquire specific receptors in a random assembly process that helps the body prepare to fight different enemies, including a multitude of viruses and bacteria. Dr. Xiao compared the assembly process to handing soldiers different kinds of weapons—a rifle for one soldier, a bayonet for another. Normally, the body also has a system of B-cell tolerance checkpoints in place to eliminate self-reactive B-cells, which attack not only viruses and bacteria, but also the body’s own tissues. This process, which relies on apoptosis (programmed cell death), seems to go awry in patients with autoimmune diseases. “For some reason, their self-reactive B cells have not been purged,” said Dr. Xiao.
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