Researchers have a new clue to what causes multiple sclerosis (MS), a disease in which the immune system destroys the protective sheath around nerve cells. A study in the January Nature Medicine suggests that in MS, immune cells never learn properly to avoid a certain protein in the duct. The results can help to pave the way for better treatment strategy.
In MS, which affects about 1 million people worldwide, the immune system eats away the fatty myelin that insulates nerves and helps in the transmission of the signal. The victims cope with episodes of muscle weakness and numbness; in severe cases, MS can lead to paralysis and death
Most of the time the immune system learns to distinguish between "self" proteins and "non-self" :. T cells, for example, going to school in the thymus, where they own baited with body proteins. These T cells that attack are eliminated. Flaws in this educational program could be a means by which autoimmune disorders such as MS might arise, thought immunologists Ludger Klein and Bruno Kyewski the German Research on Cancer in Heidelberg. For example, if there is not enough of a particular protein in the thymus, T cells that are prone to attack it would not be eliminated. To test this hypothesis, the researchers examined the activity of the gene for a protein called PLP - a major component of myelin and one of the main targets of renegade T cells in MS - in the thymus of two different strains of mice, one sensitive and one resistant to a disease similar to MS. They found that the two strains had roughly the same amounts of PLP in their thymus -. Although the version in the thymus was slightly shorter than that produced in the central nervous system (CNS)
When the team took a closer look the parts of the protein that T cells locked on during their attack, they were a surprise: in the MS-resistant strain, the top four all target regions was in the short version of the PLP present in the thymus, but in susceptible mice, a target region fell into short away section in the thymus, but present in the CNS. Like mice, humans are only the shorter version of PLP in the thymus.
To exploit this in therapy for MS, "should restore tolerance against [protein snippets], which are not expressed in the thymus" early in the course of the disease, said Stanford immunologist Lawrence Steinman. If the first results in animal work in humans as well, he added, it might one day be possible to give MS T cells with some remedial training by injecting fragments of artificial proteins.
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