Females of certain species — like humans and mice — have a known ability to produce more of the gene Kdm6a than males because it’s located on the X chromosome, of which females have two. Kdm6a is also quite active in immune system T-cells, a study found, and silencing it in a mice model of multiple sclerosis (MS) led to fewer disease symptoms, and lesser inflammation and damage to the spinal cord.
These findings may help to explain why women are more prone to MS and other autoimmune diseases than men, its researchers said. They also recommended more study into the diabetes medication metformin, which targets Kdm6a and might be the reason it shows an ability to modulate the immune system.
The study, “The X-linked histone demethylase Kdm6a in CD4+ T lymphocytes modulates autoimmunity,” was published in the Journal of Clinical investigation.
A woman’s risk of developing MS is about three times greater than a man’s, a difference that research suggests might be due to differences in sex hormones (estrogen and testosterone), in genes located on the X and Y sex chromosomes (which contain the DNA of a cell), or through a combination of the two.
Chromosomes inherited from a child’s parents determine its biological sex; women have two X chromosomes, and men have one X and one Y.
Females, however, need only one active X chromosome to be healthy. Their bodies naturally deactivate one X chromosome to avoid producing excessive amounts of the genes that it carries. Nonetheless, some genes bypass such inactivation, resulting in their higher expression in women compared to men. (Gene expression is the process by which information in a gene is synthesized to create a working product, like a protein.)
Researchers at the University of California, Los Angeles hypothesized that X chromosome genes that bypass being silenced might be related to the higher risk of autoimmune diseases seen in women.
They analyzed genes that were more expressed in immune T-cells of healthy controls (294 women and 205 men), as well as in female and male mice.
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