Press releases
Please quote Nature Immunology as the source of these items.
The November 2008 issue of Nature Immunology is available online.
November 2008
Survival strategies
Scientists have discovered a molecule that helps activated immune cells survive in the face of massive amounts of the antimicrobial signalling protein, interferon-gamma. A paper online this week in Nature Immunology suggests the molecule Irgm1 is critical to allow continued immune responses in the face of chronic infections, such as those seen in many parasitic diseases.
Interferons are antimicrobial compounds that help eradicate viruses and other intracellular pathogens. High concentrations of interferons are toxic to nearby cells. Hence it has always been a dilemma as to how those immune cells that make interferon-gamma in response to infection can themselves survive.
Carl Feng and colleagues identify a molecule called Irgm1 that plays a key role in this process—protecting immune cells that produce interferon-gamma from succumbing to its toxic effects. They show that immune cells from mice lacking Irgm1 fail to multiply and instead undergo a form of cellular suicide upon exposure to interferon-gamma. Fewer immune cells result in uncontrolled infections and all of the mice died from their infection. Mice lacking both Irgm1 and interferon-gamma survive infection, showing that Irgm1 protects these immune cells from the toxic effects of interferon-gamma.
The immunity-related GTPase Irgm1 promotes the expansion of activated CD4+ T cell populations by preventing interferon-γ-induced cell death
Carl G Feng, Lixin Zheng, Dragana Jankovic, André Báfica, Jennifer L Cannons, Wendy T Watford, Damien Chaussabe, Sara Hieny, Patricia Caspar, Pamela L Schwartzberg, Michael J Lenardo & Alan Sher
Published online: 21 September 2008 | doi 10.1038/ni.1653
Complement enhances tumour evasion
A seemingly illogical link between activation of immune sensors and the ability of tumours to escape the immune system is reported online this week in Nature Immunology. The unexpected result reveals a new drug target for cancer treatment.
The complement system comprises a cascade of proteins that act as a fire alarm to alert the immune system to the presence of infection. In a bizarre twist, Lambris and colleagues show that tumour activation of one of the complement proteins—C5—in fact leads to suppression of the anti-tumour immune response.
The surprising outcome is explained by the observation that the activated protein recruits 'suppressor' cells to the site. These act to disarm other immune cells and stop them from killing the tumour. Importantly, the authors show that blocking the activity of C5 slows tumour growth in mice and this treatment is as effective as taxol, a commonly used anti-cancer drug.
Modulation of the antitumor immune response by complement
Maciej M Markiewski, Robert A DeAngelis, Fabian Benencia, Salome K Ricklin-Lichtsteiner, Anna Koutoulaki, Craig Gerard, George Coukos & John D Lambris
Published online: 28 September 2008 | doi 10.1038/ni.1655
