MS (muscular dystrophy) is a type of disease that depletes the fatty sheaths that protect nerve fibres, causing a loss of muscle control. In the 1970s, scientists found that a specific version of a gene conferred a fourfold increase in the risk of MS. This gene encoded for an immune system protein called human leukocyte antigen DRB1.
Recently, studies in the USA and Sweden have now indicated that people with MS are 20-30% more likely than non-sufferers to have a variation of other immunity-linked genes. These genes encode the protein interleukin-2 receptor alpha, and also the receptor for the immune system messenger protein, interleukin-7.
The interleukin-7 receptor is attached to the membrane of cells, most typically immune system T-cells. When the interleukine7 binds to it, the receptor signals the cell to take part in immune response reactions.
The variant of the interleukin-7 receptor gene slightly favours production of a free-floating version of the receptor. The membrane-bound receptors compete with free-floating receptors for interleukin-7, therefore an excess of these free-floating receptors affects the fine-tuning of immune responses.
Previously, MS was believed to have a hereditary component, however the recent discovery of more MS-conducive gene variations may also indicate that MS is an autoimmune disease. This is because interleukine-2-receptor-alpha (a protein produced by one of the gene-variants) has been linked to Graves’ disease and type1 diabetes, which have autoimmune traits.
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