FRIDAY, SEPTEMBER 30, 2016

Immune system fights viruses and bacteria differently

Researchers from the U.K. discovered an important difference in the way the human immune system responds to viral and bacterial pathogens, according to a study recently published in Nature Immunology.

The research team from the University of Nottingham found that STAT1, a human protein that is able to bind DNA, acts differently depending on whether the immune system encounters bacterial or viral pathogens. STAT1 responds to interferon signals, hormone-like molecules that control communication between cells to trigger the immune system.

The researchers found that when they bred mice to express a mutated form of STAT1 which was limited to forming single STAT1 units instead of chains, the mice were unable to develop an immune response to bacterial infections. An immune response against a viral infection was not impacted by the mutated STAT1.

"The core of these findings is that we are revising a central aspect of what we thought we knew about how these proteins worked," Uwe Vinkemeier, the leader of the study, said. "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."

Type I interferons, which are involved in the antiviral response, also work to stop cells from growing and replicating. Type I interferons are in clinical use against several cancers, the hepatitis virus and in treating autoimmune diseases. Type II interferons were previously shown to be detrimental to some of these conditions, 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 anti-viral protection, intact. This would avoid an important shortcoming of current STAT1 inhibitors."