Dead gene halts inflammation Researchers have identified a single gene that controls inflammation, accelerated aging and cancer

 Agene long presumed dead comes to life under the full moon of inflammation, Stanford University School of Medicine scientists have found. 

    The discovery, described in a study to be published in eLife, may help explain how anti-inflammatory steroid drugs work. It also could someday lead to entirely new classes of anti-inflammatory treatments without some of steroids' damaging side effects. 
    Chronic inflammation plays a role in cancer and in autoimmune, cardiovascular and neurodegenerative diseases. 
WARNING SIGN 
When pathogens such as viruses or bacteria invade our body, the immune system reacts by producing a flurry of chemical signals that call specialized defender cells to the scene. This first line of defence is known as inflammation. "It is a necessary defence mechanism — you can't live without it," said Sourav Ghosh, lead author. 
To be effective against pathogens, yet prevent collateral damage from body's own defences, the immune system has to maintain just the right level of inflammation, explained Ghosh. 
    Vertebrates have two powerful lines of defence: a non-specific, or innate, immune response and the specific, or adaptive, immune response. In the non-specific response, the immune system throws a first wave of measures at the intruders, ing of aggressive destructive enzymes kamikaze-like neutrophils. don't know who the enemy you fire everywhere with eyes closed," Ghosh "But once you know, you shut this off and bring in cial ops so to speak." 
    This is specific immunity, ble of targeting pathogens cisely, while sparing microbes and cells belonging the body. "Once activated, has to be a mechanism that vents adaptive response going into overdrive," he 
PROTEIN S 
Two immune cells that used Protein S to communicate 'ceasefire' turned out to be the key players in mediating the immune response. The findings could help scientists develop treatments for inflammatory diseases by designing substitute for insufficient Protein S. According to Ghosh, patients with inflammatory bowel disease are 20 times more likely to develop colon cancer, underlining the significance of this study. 
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