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Researchers have identified a genetic clue as to why some people are immune to the tuberculosis bacterium whereas others develop the disease.

Their findings suggest that a mouse gene — of which humans have a version — confers immunity by stopping the bacterium from replicating and by altering the way cells die in response to infection.

The team, led by Igor Kamnik of the US-based Harvard School of Public Health, published their results in this week's issue of Nature.

One-third of the global population is infected with Mycobacterium tuberculosis, but only one in ten of those infected develop tuberculosis. The difference suggests that genetic factors could control a person's ability to resist the infection.

Kamnik and his colleagues had previously identified a section of DNA that made a strain of inbred mice particularly susceptible to infection by M. tuberculosis.

In their latest research, they replaced this segment with the corresponding one from mice that are naturally resistant to the bacterium. They found that the ability to resist infection was transferred with the segment of DNA.

The team found that a gene called Ipr1 found in the transferred DNA conferred resistance by limiting the replication of M. tuberculosis. The gene also appeared to change the way in which cells of the immune system died as a result of infection.

In the resistant mice, these cells, known as macrophages, died by a form of 'cell suicide' that the body uses to control cell death.

In mice that were susceptible to infection, however, macrophages died by an uncontrolled process that could make it more difficult to control the spread of the bacteria.

The human equivalent of the mouse Ipr1 gene is called SP110. The researchers suggest testing SP110 to see if it conveys resistance to the tuberculosis bacterium in humans.

In an accompanying commentary in Nature, Nada Jabado and Philippe Gros, of McGill University in Canada, say the results could help design new tuberculosis drugs.

"These studies not only provide insight into a novel aspect of TB [tuberculosis] pathogenesis, but, if validated in humans, may reveal new molecular targets for drug treatments," they write.

Link to full paper in Nature

Link to accompanying article in Nature

Reference: Nature 434, 767 (2005)

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