NEW YORK (Reuters Health) - Researchers have identified a gene that mediates innate immunity to tuberculosis in mice, according to a report in the April 7th issue of Nature. A human homologue of the gene exists and may play a similar role, they suggest.
Each year, about 8 million people become infected with Mycobacterium tuberculosis, senior author Dr. Igor Kramnik, from the Harvard School of Public Health in Boston, and colleagues note. However, only 10% of infected individuals develop tuberculosis.
Along with factors such as stress and malnutrition, another possible contributing factor is genetic variation within the host population, Dr. Kramnik’s group notes. Perhaps some individuals have genetic variants that render them more or less susceptible to clinical disease following infection.
Dr. Kramnik’s team previously identified a genetic locus, designated sst1 for super susceptibility to tuberculosis, which influences tuberculosis susceptibility in mice. In the present study, the researchers show that a gene within the locus, called Ipr1 for Intracellular pathogen resistance 1, seems to be a key mediator of susceptibility.
Ipr1 expression was increased in macrophages resistant to M. tuberculosis. By contrast, macrophages susceptible to the pathogen did not express the gene. Further analysis showed that Ipr1 expression limited the multiplication of Listeria monocytogenes as well as M. tuberculosis and forced infected macrophages to undergo apoptosis.
“Our data indicate that the Ipr1 gene product might have a previously undocumented function in integrating signals generated by intracellular pathogens with mechanisms controlling innate immunity, cell death and pathogenesis,” the authors conclude.
Source: Nature 2005;434:767-772. [ Google search on this article ]
MeSH Headings:Animal Diseases: Biological Sciences: Biology: Disease Models, Animal: Gene Expression Regulation: Genetics: Genetics, Biochemical: Immunity, Natural: Molecular Biology: Biological Sciences: DiseasesCopyright © 2002 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon. Reuters and the Reuters sphere logo are registered trademarks and trademarks of the Reuters group of companies around the world.
