One Step Closer to Personalized Medicine: Researchers Find First Bio-Marker for MS

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Researchers at the University of Alabama at Birmingham (UAB) have found the first bio-marker for multiple sclerosis (MS) that might predict which patients will respond to a standard therapy and which will not.

In findings published online March 28 in Nature Medicine, the UAB team, in a joint effort with researchers at Stanford University, discovered that patients with a particular type of T helper immune cells responded well to interferon-ß, the usual first-line therapy for the disease, while those with a different T helper immune-cell type either did not respond or experienced worsening symptoms.

“Interferon-ß is typically the first therapeutic choice for most MS patients, but there is a subset of about 30 percent of patients for whom it does not work and may make the patient worse,” said Chander Raman, Ph.D., associate professor in the Division of Clinical Immunology and Rheumatology and lead investigator of the study. “Our findings, in both animal and human models, indicate that the type of T helper cell present is the determining factor in predicting whether interferon-ß will be effective.”

Raman suggests this might be another rung on the ladder leading to personalized medicine, in which therapies are based on an individual’s physiology and genetic makeup and the nature of disease.

“When our findings are verified in an expanded human trial, a simple blood test could be used to determine which type of T helper cell is predominantly responsible for the disease in an MS patient, enabling clinicians to provide the proper therapy from the beginning of treatment and eliminate the guesswork,” Raman said.

Raman’s team, along with the team at Stanford lead by Lawrence Steinman, Ph.D., examined T helper Type 1 cells and T helper Type 17 cells in an animal model for multiple sclerosis. Both Th1 and Th17 cells are major initiators of MS and important in disease severity. The researchers found that interferon-ß was effective in mice with disease initiated by Th1 cells, but worsened disease initiated by Th17 cells. The findings were replicated with striking consistency in analysis of human-patient serum with relapsing-remitting multiple sclerosis, the most common form of the disease.

“This research reinforces the concept that diseases have certain signatures that help define their origin and give us glimpses of how they manifest in our bodies,” said Raman. “The more we understand these signatures, the more likely we will be able to intervene at a critical junction and design and provide therapies that lessen or cure disease.”

The research was supported by grants from the National Multiple Sclerosis Society and the National Institutes of Health.

The UAB team consisted of Raman, Patrizia De Sarno and Rodrigo Naves. The team led by Steinman was made up of Robert Axtell, Roopa Bhat, May Han, Franklin Zhong, Jim Castellanos, Robert Mair, Athena Christakos, Ilan Kolkowitz, and Liat Katz from Stanford University; others participating were Brigit de Jong from Radboud University Nijmegen Medical Center, the Netherlands; Laura van der Voort, Joep Killestein and Chris Polman from VU University Medical Center, the Netherlands; and Katia Boniface and Rene de Waal Malefyt from Schering-Plough Biopharma.

About the UAB Division of Clinical Immunology and Rheumatology
The UAB Division of Clinical Immunology and Rheumatology is internationally recognized and dedicated to pursuing new knowledge and translating research findings into more effective diagnosis and treatment of patients with rheumatic diseases.

EDITOR’S NOTE: The University of Alabama at Birmingham (UAB) is a separate, independent institution from the University of Alabama, which is located in Tuscaloosa. Please use University of Alabama at Birmingham on first reference and UAB on second reference.

Source:  University of Alabama at Birmingham

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