Gene HIP1 is a driver in inflammatory arthritis severity
A new gene associated with disease severity in rheumatoid arthritis has been identified by researchers at the Icahn School of Medicine at Mount Sinai.
The discovery could provide a new pathway for treatment and a way to measure the prognosis of patients. Rheumatoid arthritis is an autoimmune condition in which the body’s immune system starts to react against its own proteins.
Through a series of experiments–on synovial cells from the inner lining of joints in humans and animals, and in animal models of arthritis–Percio S. Gulko, MD, Chief of the Division of Rheumatology, Lillian and Henry M. Stratton Professor of Medicine (Rheumatology), and senior author on the paper were able to show that the gene HIP1 is a driver in inflammatory arthritis severity.
This is the first time that HIP1 has been implicated in arthritis severity and in cell invasiveness. The findings were published online in Annals of the Rheumatic Diseases on July 26.
Rheumatoid arthritis is a chronic disease. It can cause disability and deformation of joints and affects roughly 1 percent of the world’s population
Rheumatoid arthritis is a chronic disease. It can cause disability and deformation of joints and affects roughly 1 percent of the world’s population. Specific incidence figures for India are not available because studies have been mostly observational and too small to make population level extrapolations.
Drugs currently available to treat rheumatoid arthritis target the body’s immune response but raise the risk of immunosuppression and susceptibility to infections such as herpes zoster and pneumonia.
“There have been major advances in the treatment of rheumatoid arthritis in the past 20 years, but disease remission still remains uncommon. Most drugs today target inflammation but often that is not enough to control disease,” says Dr. Gulko.
“At my laboratory, we have been looking for alternative strategies. In this research, we have focused on understanding the regulation of disease severity and joint damage. Our discovery led us to the synovial fibroblasts, cells inside the joint,” he added.
Dr. Gulko’s research provides a framework for a potential new target for therapy and, perhaps, a new predictor of a patient’s prognosis. He and his colleagues plan in the future to investigate the feasibility of a drug that would target the HIP1 gene.
