New research offers clues to the causes of multiple sclerosis and may offer a path toward designing more specific treatments.
Multiple sclerosis —an autoimmune disease in which immune cells strip the protective myelin insulation from nerves—has long puzzled researchers. One key mystery is which of the body’s immune cells go rogue—and why. Now, a new study suggests that as some T cells set out on their path of destruction, they swipe a critical protein from another type of immune cell, called B cells. Targeting these larcenous T cells could open the door to new MS therapies with fewer side effects.
In earlier research, scientists had noticed a rare subset of T cells that carry CD20. Although these cells occur in healthy people, they are more abundant in patients with MS, and lab studies suggested they could be particularly destructive. Yet how these T cells end up with CD20—which is a defining feature of B cells—and how they promote nerve damage in MS remained unclear.
Weber and colleagues set out to test that explanation using cells from healthy mice. First, they grew the animals’ B cells together with T cells that had no CD20 in a lab dish. Sure enough, after 1 to 2 days,. But when there was a barrier between the two types of cells, the T cells remained CD20-free. That suggests the T cells need “direct and close molecular contact” to pick up the protein, Weber says. The researchers obtained similar results when they grew human T and B cells together.
The study also bolsters the case that these rogue T cells are helping wreak destruction in MS. The researchers determined that T cells with CD20 produced more inflammation-stimulating molecules than did cells without the protein, for instance. They also outfitted their membranes with more of the sticky proteins that can help them slither into nerves, where they could cause damage.
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