HOUSTON Scientists have identified an influential link in a chain of events that leads to autoimmune inflammation of the central nervous system in a mouse model of multiple sclerosis (MS).
An international team of researchers led by scientists in The University of Texas MD Anderson Cancer Center Department of Immunology reported their results in an advance online publication in Nature Medicine.
The researchers spell out the pivotal role of Peli1 in the activation of immune cells called microglia that promote inflammation in the central nervous system in response to tissue damage or invasion by microbes.
"The major implication of discovering a signaling role for Peli1 in this animal model is that it might also be significant in the pathogenesis of MS," said senior author Shao-Cong Sun, Ph.D., professor in MD Anderson's Department of Immunology.
Microglia cells involved in multiple sclerosis
Sun and colleagues found that Peli1 is heavily expressed in microglial cells and promotes their activation and subsequent damaging immune response. Peli1 also protects that autoimmune reaction by initiating the destruction of a protein that otherwise would inhibit inflammation.
Microglia are known to be crucial to the initiation of MS, an immune system assault on nerve fibers called axons and on myelin, the protective sheath around the axons. They also were previously known to play a similar role in experimental autoimmune encephalomyelitis (EAE), an animal model of MS.
The precise mechanism of this autoimmune-stimulating effect has been unknown. Sun and colleagues fill an important gap with their Peli1 discovery.
Microglia sense tissue damage. They secrete chemokines and inflammatory cytokines in response, drawing infection-fighting T cells into the central nervous system, leading to inflammation.
Infections genetic overreaction that inflames
The authors note that microbi
|Contact: Scott Merville|
University of Texas M. D. Anderson Cancer Center