Press releases
Please quote Nature Immunology as the source of these items.
The October 2008 issue of Nature Immunology is available online.
October 2008
Coping with immune cell death
Researchers have discovered a 'sensor' molecule that alerts the immune system to the presence of necrotic cells. The work, described online this week in Nature Immunology, shows how the body prevents excessive inflammation caused by non-infectious injuries and prevents uncontrolled tissue damage.
Poisons, ultraviolet light, radiation and other non-infectious injuries can lead to inflammation and necrosis—the unnatural death of cells and tissue material. Takashi Saito and colleagues find that a receptor molecule called Mincle, expressed by macrophages, functions as a direct sensor for this type of cell death.
Mincle detects internal components of necrotic cells that are released into the surrounding milieu. This drives macrophages to produce a chemical signal, interleukin 8, that promotes infiltration of white blood cells called neutrophils into necrotic tissues. The neutrophils then help resolve inflammation caused by the necrotic debris.
Mincle is an ITAM-coupled activating receptor that senses damaged cells
Sho Yamasaki, Eri Ishikawa, Machie Sakuma, Hiromitsu Hara, Koji Ogata & Takashi Saito
Published online: 07 September 2008 | doi 10.1038/ni.1651
The tuberculosis bacterium's stealthy ways
Mycobacterium tuberculosis—the bacterium that causes most cases of tuberculosis—spreads infection by blocking a naturally triggered immune response that would cause the infected cells to die. The research, published online this week in Nature Immunology, provides possible new avenues for designing inhibiting drugs to prevent mycobacterial diseases.
Mycobacteria tuberculosis infects immune cells called macrophages, which function as temporary 'incubators' while the bacteria multiply. Eventually the macrophages burst, releasing the bacteria to infect other cells. Normally macrophages infected with bacteria would undergo a form of cell death called apoptosis and trigger an immune response.
Heinz Remold and colleagues found that M. tuberculosis prevents macrophages from undergoing apoptosis. Instead, M. tuberculosis caused macrophages to die by necrosis, another form of cell death that allows the bacteria to escape from their host cells and infect new cells. By revealing how M. tuberculosis can evade the immune system this study provides significant insight into the development of tuberculosis disease.
Mycobacterium tuberculosis blocks crosslinking of annexin-1 and apoptotic envelope formation on infected macrophages to maintain virulence
Huixian Gan, Jinhee Lee, Fucheng Ren, Minjian Chen, Hardy Kornfeld & Heinz G Remold
Published online: 14 September 2008 | doi 10.1038/ni.1654
