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Scientists learn the origin of rogue B cells

that about 10 percent of the body's B cells retain both receptors: a good, useful one and the faulty self-reactive one that the good receptor was designed to replace. This means that the aberrant B cells have escaped the body's mechanism to correct them. "Our research goes against the theory that B cells should only express a single receptor," says Casellas.

Using a technique in which they inserted a piece of human gene into the cells of laboratory mice, the researchers created a model for visualizing the process in live animals. "Most of what scientists do is to create systems to visualize complex phenomena, then to allow nature to give you the answers to your questions," says Casellas.

Their new findings raise the question of how this knowledge might eventually help people with autoimmune disease. That question, says Casellas, is one that will take time to answer. "This is only one step," he says. "We all carry these cells around, but not all of us develop autoimmunity. Our work provides one explanation for the origin of these self-reactive B cells."

"If you understood the system extremely well and were able to delete the editing cells during development, for instance, then you would only have lymphocytes that don't express self-receptors at all," he says.

For now, the step forward to understand where these self-directed cells are coming from is a big one. "Our objective is to understand the ins and outs of this process," says Casellas.


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Source:NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases


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