A study, published in the Journal of Experimental Medicine, has identified a small genetic change that increases the odds of developing active tuberculosis.

Pedro Flores-Villanueva and his colleagues at the University of Texas Health Center studied groups of patients in Mexico and Korea and found that individuals who carry this genetic change were more likely to develop disease when infected with tuberculosis -causing bacteria.

Infections with Mycobacterium tuberculosis, the bacterium that causes tuberculosis, are on the rise, with an estimated eight million new infections and two million tuberculosis -induced deaths occurring annually.
But not all people who are exposed to this bug become ill -- a phenomenon largely explained by genetic differences that make some individuals more prone to developing disease than others.

Indeed, a recent scientific study found that a particular region on the human chromosome 17 was associated with increased risk of developing active tuberculosis, but the exact gene(s) responsible for this effect was not identified.

Flores-Villanueva and colleagues show that the culprit behind the increased susceptibility to tuberculosis was a small change in the gene that encodes a protein called MCP-1 ( the MCP-1 gene resides of chromosome 17 ).
The genetic change was a tiny one, with the DNA sequence differing by only a single nucleotide.
This change, which resulted in increased production of the MCP-1 protein, was five times more prevalent in individuals with active tuberculosis than in those who were infected but remained healthy.

MCP-1 is a protein that helps attract immune cells to sites of infection.
For this reason, this protein is important during the early immune response to tuberculosis -causing bacteria.
But extremely high levels of MCP-1 can be dangerous, as they inhibit the production of another immune protein called interleukin-12.
Interleukin-12 is required to activate the immune cells that fight off the infection once they arrive on the scene.

Source: Journal of Experimental Medicine, 2005


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