Researchers have identified a gene in mice that regulates immunity to Tuberculosis. An equivalent gene exists in humans and may play similar role, they suggest.

Each year, about 8 million people become infected with the bacterium that causes TB, Myobacterium tuberculosis, note Dr. Igor Kramnik, from the Harvard School of Public Health in Boston, and colleagues in the research journal of Nature. However, only 10 percent of infected individuals develop tuberculosis.

Along with factors such as stress and malnutrition, genetics may contribute to the odds of developing actual TB, Kramnik’s group believes. Perhaps, they say, some individuals have genetic variants that render them more or less susceptible to clinical disease following infection.

The team previously identified a genetic region, designated sst1 for “super susceptibility to tuberculosis,” which influences tuberculosis susceptibility in mice. In the current report, the researchers show that a gene within the sst1 location, called Ipr1 for “intracellular pathogen resistance,” seems to be a key moderator of susceptibility.

Ipr1 expression was increased in cells resistant to M. Tuberculosis infection. By contrast, cells susceptible to the bacterium did not express the gene.

Further analysis showed that Ipr1 forced infected cells to commit suicide, thus preventing TB from gaining a foothold.

SOURCE: Nature, April 7, 2005.