A paper published recently in Science Immunology details the double role of an immune system molecule called USP18. The molecule helps curtail immune response, but can also open the door to infections by bacteria such as listeria and staph.
Type I interferon (IFN-I) signaling is known to impair host immune responses during many primary and secondary bacterial infections. Scripps Research scientists were trying to understand this apparent paradox and determine how interferon-stimulated genes (ISGs) that usually help fight against viruses also dampen ability to resist many bacterial infections.
In the current study, the researchers deleted USP18, a single type of ISG, in mouse dendritic cells. This action enhanced the body’s ability to control infections with two strains of Gram-positive bacteria. They also found that normal induction of USP18 after infection impaired antibacterial responses mediated by tumor necrosis factor release.
"Our results were unexpected because the absence of USP18 augments type 1 interferon signaling, which, if the current thinking is correct, should promote rather than prevent bacterial infection," said study senior author John Teijaro, PhD, assistant professor at Scripps Research,.
The researchers note that these findings add to basic understanding of the immune system and may offer a target for future drug therapies to treat bacterial infections.