Approximately eight million people worldwide are infected with TB annually, with an estimated two million people dying from the lung disease each year. TB is caused by the pathogen Mycobacterium tuberculosis, but infection does not automatically result in full-blown disease. In the U.S., minority and foreign-born populations have significantly higher rates of TB than the overall U.S. average, according to the Centers for Disease Control and Prevention. In 2004, African Americans had TB case rates that were eight times higher than whites.
Scientists have understood that mice -- a frequently used animal model in experiments -- combat microbes such as TB by producing nitric oxide in scavenger cells of the immune system known as macrophages. However, this mechanism is not prominent in humans, and the mechanism by which human macrophages kill the tubercle bacillus has remained an additional puzzle. Innate immunity is the rapid immune response of host scavenger cells to recognition of certain patterns of molecules found on pathogens, which has been retained in evolution from fruit flies to humans. A set of receptors on macrophages in humans called Toll-like receptors contribute to innate immune responses. The researchers describe a novel pathway used by human macrophages that may be critical to resisting infection with certain pathogens and that turns out to be critically dependent on vitamin D. This description provides a different way to think about how human immune systems battle pathogens in
Contact: Robin Herman
Harvard School of Public Health