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.