A study at Penn University explains female susceptibility to autoimmune diseases.
Females have two X chromosomes which lets them off easy as far as infectious diseases are concerned. However, they are also more susceptible to autoimmune problems such as lupus.
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The study was published in Proceedings of the National Academy of Sciences and led by researchers from the University of Pennsylvania. This new study points the way forward in this regard. It seems that X inactivation is the name of the game.
Gene expression on one of the two X chromosomes of the female shows this tendency. In case of females, the immune system’s lymphocytes, in particular T cells and B cells, don’t have the repertoire of Xist which is an RNA molecule necessary for inactivation.
It is also needed for other issues having to do with X chromosome inactivation. Therefore X inactivation remains a curtailed process in these cells.
All female patients showed inactivation patterns in their lymphocytes. As for the lupus patients among them, they showed a singular expression of immunity-related genes. The style of RNA localization was also odd.
Thus there was an interior reason for the appearance of the disease in the females. The gist of the matter is the lymphocytes. Quietening the X chromosome in them is not an easy job to accomplish.
The study originated in the X inactivation of pluripotent stem cells. What role Xist plays in all this is important. Xist is a lengthy non-coding RNA molecule that inactivates X chromosomes.
Repression of gene activation occurs thanks to heterochromatic modifications. In some of the cases, the stem cells lose both the Xist expression and the modifications.
Reactivation is the normal result of this state of affairs. The resulting growths then begins to resemble cancer cells in their makeup.
Since 85% of lupus sufferers are women, this gene expression seems to be a particular feature of X chromosome activation. The autoimmune condition is a female affliction.
The issue is that Xist does not shift to the inactive X in order to dampen it. Similar results were seen in mice. The problem was not the Xist. There were tons of this material in the cells.
The real conundrum lay in the fact that the Xist was not shifting over to the inactive X chromosome in the lymphocytes. Even the heterochromatic marks were noticeable by their sheer absence.
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Thus even healthy females had the potential of contracting autoimmune diseases such as lupus. Therefore Xist could be taken as an early biomarker that may be manipulated in the future to counter the disease.