In the dead of winter, so many of us visit the doctor expecting a prescription for whatever ails, whether bacterial or not. Now, a team of scientists in the United Kingdom says they’ve discovered a key difference in how the body’s immune system responds to bacterial and viral pathogens, alike.
Lead investigator Uwe Vinkemeier and his colleagues focused on a protein known as STAT1, whose ability to bind to DNA means a vital role in regulating genes throughout the body. The protein answers the call of interferon signals, those hormone-like molecules controlling inter-cellular communication when challenged by bacterial and viral pathogens, as well as parasites. The same system also helps to fight tumor growth, in many cases completely eviscerating the cancer.
On Sunday, the British team announced a new understanding of the protein’s role in preventing disease. Previously, scientists had thought that all interferons used units containing a single copy of the protein, as opposed to assembled chains of STAT1 protein, to regulate gene activity. However, they found that some interferons (type II) were rendered useless against bacterial pathogens when the molecular assembly of protein chains was inhibited in the mice.
"The core of these findings is that we are revising a central aspect of what we thought we knew about how these proteins worked,” Vinkemeier said in a statement. “The molecular mechanisms underlying type I and type II interferon functioning are actually more distinct than we previously imagined. This in turn offers new options for rational pharmacological intervention."
Already, pharmaceutical companies offer drug treatments for Hepatitis virus and several cancers based on type 1 interferons known for antiviral and anti-cancer responses. However, type II interferon, useful in the body against bacterial invaders, has been shown harmful in some cases, including multiple sclerosis and melanoma.
"In situations like these our finding offers a new target for making current treatments more effective,” Vinkemeier said. “There is good reason to assume that an inhibitor of STAT1 chain formation could potentially block detrimental type-II interferon responses while keeping type I activities, including antiviral protection, intact. This would avoid an important shortcoming of current STAT1 inhibitors."
Source: Uwe, Vinkemeier. Research Uncovers Keys Difference Between Our Bodies’ Fight Against Viruses And Bacterial. Nature Immunology. 2013.