According to a publication from EurekAlert, a study recently published in the medical journal Nature Genetics suggests how certain immune cells express genetic activity similar to that of variations of the human genome associated with greater risk of developing an autoimmune disease.
About Autoimmune Diseases
There are over 100 unique autoimmune conditions, all similarly characterized by overactive immune systems that mistakenly damage healthy tissues and organs as though they were bacterial, viral, or fungal pathogens.
Autoimmune conditions may not have singular identified causes — they may be triggered by genetic or unknown environmental factors, or some combination of the two.
Certain “normal” versions of hundreds of genes are associated with more frequent development of autoimmune disease. These “genetic variants” are intensely researched as a popular focus of genetic medical research.
How Certain Immune Cells Resemble Genetic Variants
Researchers from the United Kingdom’s Sanger Institute sampled 3 types of immune cell from a number of healthy volunteers. Institute researchers then identified what parts of the genome were being expressed by these immune cells by comparing those profiles against a number of previously identified genetic variants associated with autoimmunity.
A number of cell messengers, called cytokines, were artificially introduced to these immune cells to create 55 unique cell states simulating various stages of autoimmune inflammation.
Of the three types of cells tested, memory T cells were found to have the genetic profiles most similar to those “genetic variants” associated with autoimmune diseases. Specifically, researchers were surprised to find that it was the early activation of these memory T cells that had the most overlap with genetic variants.
The finding implies that the early activation and activity of memory T cells may have bearing on the future development of autoimmune dysfunction.
Dr. Gosia Trynka, the senior author on the Sanger Institute study, acknowledged the difficulty of identifying potential causes of autoimmune disease. Calling the effort “like finding a needle in a haystack,” Trynka wasn’t long to linger on the impressive conclusions of this study. By using the Sanger study as a springboard for future research into the role of memory T cells in autoimmunity, Trynka hopes to identify various genes and biological pathways that could act as targets for drug therapies.
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