For the first time, scientists from Umeå University have shown the importance of DNA damage in fine-tuning our innate immune system and hence the ability to mount the optimal inflammatory response to infections and other biological dangers. The study was published in the February 17, 2015 issue of Immunity. The title of the article is “DNA Damage Primes the Type I Interferon System via the Cytosolic DNA Sensor STING to Promote Anti-Microbial Innate Immunity.” The research group of Dr. Nelson Gekara, within the Laboratory for Molecular Infection Medicine Sweden (MIMS) at Umeå University, is interested in understanding how the innate immune system, our first line of defense, is regulated and how defects in the innate immune system contribute to infectious and inflammatory diseases. Our immune system does not lie idle waiting to be attacked before it responds. Even in the absence of infections, our immune system is in a constant state of alert. Among the immune mediators that are constantly produced at low levels, and that keep our immune system awake, are a group of factors called type I interferons. A very delicate balance in the production of type I interferons is essential for health: insufficient production results in susceptibility to viral infections, while excessive production normally leads to autoimmune/inflammatory diseases. One of the questions Dr. Gekara´s lab has been investigating is aimed at understanding the signaling processes that control type I interferon production and, in particular, to identify the endogenous "danger signals" that constantly trigger basal production of interferons and therefore keep our immune system in a "ready-to-attack" state. The clue to answering this question came from a rare, but complex disease called ataxia telangiectasia (AT).
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