The Rheumatology Research Foundation each year highlights some of the innovative projects funded by the organization during a special session. This year, three investigators will present new insights into the pathogenesis, diagnosis, and treatment of rheumatoid arthritis (RA).
Innovative Research: A Rheumatology Research Foundation Special Session will take place from 7:30 – 9:00 am on Wednesday in Room 28 A-E. Presenter and Scientific Advisory Council Chair for the Foundation Timothy B. Niewold, MD, said he looks forward to this session every year.
“The Rheumatology Research Foundation is the largest private funder of rheumatology research,” he said. “We really want to show Annual Meeting attendees the exciting research made possible by the Foundation.”
Dr. Niewold, Judith and Stewart Colton Professor of Medicine and Pathology at New York University School of Medicine, will share one exciting project during his presentation, “Type I Interferon as a Predictor of Anti-TNF Response.”
“There are a lot of medication choices now for rheumatoid arthritis, but we still don’t really know which ones to choose for a particular patient,” he said. “It’s been wonderful that we’ve seen a lot of drug development, but as a result, we often spend a lot of time cycling through different drugs to find the one that will work well.”
Dr. Niewold said the research team was particularly interested in looking at the TNF inhibitors.
“There are probably 30 percent of patients for whom TNF-inhibitors are the perfect thing,” he said. “Unfortunately, there are another 30 percent of patients who do not get much out of them at all. This is important because we know it’s crucial to get control of the rheumatoid arthritis disease process as early as possible. We know that the longer it remains uncontrolled, the more joint damage someone will accrue over time.”
He said he hopes his research will someday help clinicians avoid giving ineffective drugs to patients. That will reduce the risk of joint damage and be more cost effective.
The investigation began with data that suggested that the level of type 1 interferon a person had might be useful in predicting response to TNF-inhibitors.
“Different people have different levels of type 1 interferon, and it probably marks people with some differences in their immune systems,” Dr. Niewold said. “We had a good assay for this in the lab, and we connected with people who had large patient sample collections.”
The collections included samples from before patients started treatment, and patients were followed to see if they responded to TNF-inhibitors. Investigators found that an increase in interferon beta was predictive of not responding to TNF-inhibitors, he said, and it performed strongly in both a test cohort and a validation cohort.
The research team is now conducting a second phase of the study with a larger cohort and is also studying the samples to try to answer the biological question of what interferon beta does.
“This provides us with an interesting opportunity to try to see how the immune system is different in folks who don’t respond,” Dr. Niewold said. “Maybe this will give a better idea of either how the drug is working or how RA is different in different people. We started studying monocyte cells from patients with high interferon beta and patients with low interferon beta — what would be considered our response group and non-response group. We were able to find patterns of gene expression in the cells that differed and correlated strongly with the response group, so that gives us a next step. We can work backwards and try to see how these monocytes behave differently in patients with different interferon levels.”
Dr. Niewold hopes that following another large, external validation, the research may be able to be translated into clinical practice.
“The test we do in the lab to measure interferon is complicated and specialized, so there are things we’ll have to figure out before we’ll be able to mass produce it,” he said. “But those are things we can certainly overcome. In the end, the best thing we can hope for will be a composite-type test or score that will be a more useful clinical predictor than any single test from an individual project. Our test, combined with two or three other measurements, would give clinicians a really robust pre-treatment screening tool.”
The symposium will also include a presentation by Joseph E. Craft, MD, the Paul B. Beeson Professor of Medicine and Professor of Immunobiology and Program Director of Investigative Medicine at Yale School of Medicine, New Haven, CT. He will present “Studying Monocytes and iPS Cells in RA.”
Inez Rogatsky, PhD, Assistant Professor at Weill Cornell Medicine Graduate School of Medical Sciences, New York, will present “Protective Actions of Transcriptional Cofactor GRIP1 in Inflammatory and Metabolic Pathologies.”