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The Center for Molecular Medicine of the Austrian Academy of Sciences (CeMM) announces the discovery of a new molecular sensor in human cells capable of recognizing infecting viruses and transmitting an alarm signal to the body.
The study, directed by the center’s director Giulio Superti-Furga, appears today in the online advanced publication route of the journal Nature Immunology. The newly discovered protein, termed AIM2, patrols the inside of human immune cells and when it encounters a DNA that is suspicious, possibly coming from an intruding virus or bacterium, triggers the secretion of the signaling protein Interleukin-1. This proinflammatory molecule activates an anti-invasion alarm program throughout the entire body. It is one of the main causes of fever and a central mediator of autoimmune disease. Thus, the study identified a new centerpiece of the human’s defense arsenal against pathogens.
“We are excited about this molecule as it helps understand the body’s immediate reaction to infections. It is much too early to say, but in the future AIM2 could lead to ways to enhance the patients’ own protection when this is needed, as during epidemics or when otherwise immune depressed”, stresses Tilmann B?? the first author of the study.
The results derived from a large scale, systematic search for human proteins that bind pathogenic molecules. Three other groups from Worcester, Philadelphia and Adelaide report the identification of the same protein in parallel publications appearing in the journals Nature and Science. This fact stresses the importance of the discovery made at CeMM.
“I am very proud that our new research center could contribute to such a fundamental immunology finding. It shows that CeMM as an Austrian research organization competes in the top-league of international research only a few years after being founded and before entering its new building. We are eager to collaborate with our clinical partners at the Medical University of Vienna to investigate if malfunction of the protein may be associated with autoimmune disease, when too much inflammatory signals are produced”, adds Giulio Superti-Furga.
http://www.cemm.oeaw.ac.at/
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