Researchers have discovered a key difference in the biological mechanisms by which the immune system responds to viral and bacterial pathogens.
A new study led by Professor Uwe Vinkemeier from the University of Nottingham, centered on STAT1, a protein that can bind DNA and hence plays a vital role in regulating genes in the body.
STAT-1 responds to interferon signals, hormone-like molecules which control communication between cells to trigger defensive action by the body's immune system when pathogens such as bacteria, viruses, or parasites are detected.
These powerful defensive actions are also part of the body's ability to control the growth of malignant tumours that can ultimately achieve their complete elimination.
Using mice bred specially to express a mutated form of STAT1 which is limited to forming single STAT1 units, the Nottingham team has demonstrated that this abolishes the function of some interferons while leaving others largely unaffected.
They found that when the assembly of STAT1 chains was inhibited, type I interferons responsible for protecting against viruses such as vesicular stomatitis virus were unaffected, whereas type II interferons, which protect against bacterial infections such as listeria, no longer functioned effectively.
"The core of these findings is that we are revising a central aspect of what we thought we knew about how these proteins worked. 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," Vinkemeier said.
The study was published in the journal Nature Immunology.
