Cells of the immune system communicate using molecular messengers. One group of these substances are interferons. During a virus infection, the immune system increases the production of interferons such as Beta-Interferon, thus alerting immune cells to combat the infection. Furthermore, Beta-interferon also has tumour fighting qualities and – used as a therapeutic against multiple sclerosis – is of major importance for medicine. Researchers from the Molecular Immunology group at the Helmholtz Centre for Infection Research (HZI) in Braunschweig, Germany have now shown that Beta-Interferon also plays a crucial role during an immune response: without Beta-Interferon immune cells are unable to show “wanted posters” of pathogens to other cells. As a consequence, these cells will not recognize the pathogen and the immune response does not start properly. The group’s results have now been published in the current issue of the scientific magazine “Journal of Immunology”.
During an infection, immune cells produce Beta-Inferferon. Interestingly, an immune response is even stronger when a low amount of Beta-Interferon has already been present before the infection occurs. Scientists call this behaviour “priming”. A healthy basal level of Beta-Interferon facilitates a faster immune reaction against microbial and viral threads. Researchers from the HZI have now managed to show why this is the case: Beta-Interferon is a key regulator and of vital importance in enabling the immune system to display fragments of pathogens, so-called antigens. Immune cells present these antigens on their surface and in this way communicate with one another: antigens are the “wanted posters” of the virus or the bacterium which has to be destroyed.
The researchers discovered the important role of Beta-Interferon in mice lacking the gene for Beta-Interferon. These mice displayed poor immune responses. “Without those knock-out mice we would not have been able to identify the impact of Beta-Interferon on the immune system,” says Siegfried Weiß, leader of the Molecular Immunology group at the HZI. His research assistant, the scientist Natalia Zietara, investigated what Beta-Interferon is doing in immune cells. She found a molecular factor that is pivotal in producing the pathogen’s profile and which is regulated by Beta-Interferon. The factor belongs to a group of proteins that is usually produced in conditions of stress. Without Beta-Interferon, no active stress protein – without stress protein, no wanted poster – without wanted poster, no immune response.
“We now have a far better understanding of how immune responses start, but also how diseases like autoimmune diseases may develop,” says Weiß: without Beta-Interferon, the immune system may not be able to learn how to tolerate itself during the embryonic phase and that it should not fight against self-structures. “Our findings can help to develop or improve new therapeutics to combat autoimmune diseases such as multiple sclerosis or cancer.”
Originalartikel: Zietara N, Lyszkiewicz M, Gekara N, Puchalka J, Dos Santos VA, Hunt CR, Pandita TK, Lienenklaus S, Weiss S. Absence of IFN-beta impairs antigen presentation capacity of splenic dendritic cells via down-regulation of heat shock protein 70. J Immunol. 2009 Jul 15;183(2):1099-109.
