Researchers have revealed that blocking cell-surface receptor called DR3 can significantly slow or prevent inflammation in autoimmune disease without leaving the body at serious infections risk.
DR3 is a protein on the surface of cells. It is a member of the tumour necrosis factor (TNF) family of receptors, which bind to molecules related to TNF, a protein that promotes inflammation.
The team from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) conducted their study using a mouse model asthma and multiple sclerosis. They found that mice engineered to lack DR3 were resistant to these autoimmune diseases.
"The implication is that blocking DR3 in mice, and possibly in humans, is a potential therapy for these diseases and perhaps others in which the immune system goes awry," said Dr Richard Siegel, Ph.D., lead researcher and a scientist in the NIAMS' Immunoregulation Group.
"These findings open up new avenues for therapy of these two diseases as well as to other autoimmune diseases in which T cells play a role in causing or perpetuating the disease," he added.
Scientists also found that removing DR3 did not appear to suppress the immune response or the ability to fight infection within the mice - a problem with many other treatments for autoimmune disease.
"We could see the effect of DR3 deficiency in the diseased organ, but when we looked systemically at the immune response at other places in the mouse, it was barely affected," said Dr. Siegel.
The researchers hope that DR3-blocking agents will be effective anti-inflammatory treatments someday.
The study is published on line in the journal Immunity.