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ScienceDaily (July 1, 2009) — Scientists have uncovered new evidence suggesting that damage to nerve cells in people with multiple sclerosis accumulates because the body's natural mechanism for repair of the nerve coating called "myelin" stalls out.

The study, published July 1, 2009, in the print edition of Genes & Development, was conducted by scientists at the University of California, San Francisco and University of Cambridge. The research was led by co-senior investigator David Rowitch, MD, PhD, a Howard Hughes Medical Institute investigator at UCSF.
The investigation, conducted in mice and in human tissue, showed that repair of nerve fibers is hampered by biochemical signals that inhibit the development of cells known as oligodendrocytes, which function as repair workers in the brain.
Oligodendrocytes form a protective sheath, known as myelin, that insulates the fibrous cables, or axons, radiating from nerve cells. In multiple sclerosis, the immune system's T cells and B cells attack oligodendrocytes, ultimately damaging the myelin sheath to the point that the electrical signals transmitted by the axons beneath it are disrupted.

ScienceDaily (Mar. 4, 2007) — Macrophages are the immune cells that engulf and destroy the debris of damaged tissue to enable the healing process to begin. Their presence at the scene of damage is critical, but once their task is complete, it is just as critical that macrophages exit rapidly, ending the inflammatory process and making way for regrowth. In fact, the continued presence of macrophages could damage tissue, compromising repair.

While researchers know a great deal about the molecular machinery that launches this cellular cleanup crew into action, little has been known about the just-as-critical exit process.