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A protein called TRAF3, with a previously unknown job in immune cells, is actually a key part of a mechanism that triggers release of anti-virus molecules called type I interferons (IFNs) as part of the body’s rapid response against these invaders, according to investigators that include a scientist now continuing this work at St. Jude Children's Research Hospital.
The discovery of TRAF3’s role helps explain how immune cells called macrophages use sensing devices called Toll-like receptors (TLRs) to orchestrate just the right response to different types of infections. TLRs are on the outer membranes of macrophages and respond to germs by triggering the production of proteins called cytokines.
The researchers showed that TRAF3 is not only essential for production of type I interferons, but also for production of IL-10, a protein that prevents inflammation. In fact, the team showed that cells lacking the gene for TRAF3 cannot produce IL-10 and instead over-produce proteins that cause inflammation.
A report on these results appeared online in the November 23 prepublication issue of Nature.
"The discovery that TRAF3 is also recruited to Toll-like receptors is a big step toward solving the mystery of how macrophages can pick and choose among different strategies for combating specific infections," said Hans Haecker, MD, PhD, of the St. Jude department of Infectious Diseases, the paper’s first author. Haecker was at the Technical University of Munich and the University of California, San Diego, when he worked on this project.
Results of the study suggest that the specific type of immune response triggered by TLR signaling depends on the relative amounts of TRAF3 and TRAF6 that are initially recruited and the different signaling proteins each of those proteins subsequently recruit to orchestrate the immune response.
Last update: February 2006