Ipr1 gene mediates innate immunity to tuberculosis

Hui Pan, Bo-Shiun Yan, Mauricio Rojas, Yuriy V. Shebzukhov, Hongwei Zhou, Lester Kobzik, Darren E. Higgins, Mark J. Daly, Barry R. Bloom and Igor Kramnik ()
Additional contact information
Hui Pan: Harvard School of Public Health
Bo-Shiun Yan: Harvard School of Public Health
Mauricio Rojas: Harvard School of Public Health
Yuriy V. Shebzukhov: Harvard School of Public Health
Hongwei Zhou: Harvard School of Public Health
Lester Kobzik: Harvard School of Public Health
Darren E. Higgins: Harvard Medical School
Mark J. Daly: Whitehead Institute for Biomedical Research
Barry R. Bloom: Harvard School of Public Health
Igor Kramnik: Harvard School of Public Health

Nature, 2005, vol. 434, issue 7034, 767-772

Abstract: TB or not TB Only about one in ten individuals infected with Mycobacterium tuberculosis actually develop clinical tuberculosis. Stress, malnutrition, concomitant infections and age all influence susceptibility, but so does genetic host resistance. A gene mediating innate immunity to tuberculosis has now been identified in mice. Expression of the Intracellular pathogen resistance 1 (Ipr1) gene in macrophages limits the multiplication not only of M. tuberculosis but also of Listeria monocytogenes. The closest homologue to Ipr1 protein in humans is the nuclear body protein SP110, so the SP110 gene is a candidate to be tested for a role in tuberculosis susceptibility.

Date: 2005
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DOI: 10.1038/nature03419

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