Protein Acts as gatekeeper in Mice Model of Arthritis

September 14, 2010

The discovery of a protein in mice sheds light on arthritis in humans, according to research published in The Journal of Experimental Medicine.

The discovery of a protein in mice sheds light on arthritis in humans, according to research published in The Journal of Experimental Medicine.

The scientists were able to eliminate a molecular protein that leads to the development of arthritis in mice. The protein acts as a gatekeeper and determines whether cells that mistakenly damage the body’s tissues, leading to autoimmune disorders, will live or die.

“This finding is an encouraging step forward for researchers, clinicians and arthritis sufferers, many of whom fail available therapies,” said lead researcher Frances Lund, Ph.D., professor of Medicine in the Division of Allergy/Immunology and Rheumatology at the University of Rochester Medical Center, in a press release. “An added bonus is that this finding may help in the search for new treatments for other autoimmune disorders, such as lupus.”

The protein is known as G alpha q and regulates B cells that fight off bacteria, viruses, and parasites, as part of the immune system. Some B cells are autoreactive and begin to cause autoimmune disorders. The research demonstrates that in mice, G alpha q stops autoreactive B cells from building up in tissues. It does so by suppressing the pro-survival signaling pathway, which was uncovered by Lund’s team.

Future research may use the findings to test compounds that work on moderating G alpha q protein levels.

“There is a subset of cardiac patients who, due to an inherited genetic mutation, have increased levels of Gαq,” Lund said, in a press release. “We are now looking to see if some arthritis patients have mutations that favor decreased levels of Gαq. If we find these patients, someday we may be able to design targeted, personalized therapy for this subpopulation of arthritis sufferers.”