About Multiple Sclerosis Foundation



Home > Learn About Multiple Sclerosis > News > Researchers implicate chemical in MS

Researchers implicate chemical in MS

4/30/2015

A new study confirms that the cytokine granulocyte macrophage colony-stimulating factor (GM-CSF) likely plays an important role in multiple sclerosis. Researchers also offer a new explanation for why the MS treatment interferon-Beta (INF-β) is often effective at reducing attacks.

Researchers, led by Abdolmohamad Rostami, M.D., Ph.D., Chair of the Department of Neurology at Thomas Jefferson University and director of its neuroimmunology laboratory, tested blood samples of patients with MS who had not yet received therapy, and those currently being treated with INF-β, a commonly used therapy. On average, untreated patients had two to three times as many immune cells producing GM-CSF as did patients being treated with INF-β, or normal subjects. Researchers looked at brain samples of deceased patients with MS and found increased numbers of GM-CSF-producing cells in comparison to normal brain samples.

“Abundant GM-CSF production at the sites of CNS inflammation suggests that GM-CSF contributes to MS pathogenesis. Our findings also reveal a potential mechanism of IFN-β therapy, namely suppression of GM-CSF production,” the authors said.

The findings were published online in the Journal of Immunology.



  Support the MSF
Supporting MSF's programs to help make "a brighter tomorrow" has never been easier.
make a donation 

  Learn About MS
Common symptoms of MS include fatigue, weakness, spasticity, balance problems, bladder and bowel problems, numbness, vision loss, tremors and depression.
learn more 

 

Unless otherwise specified, all medical content is compiled by MSF staff and reviewed for accuracy by a member of our Medical Advisory Board.

The MSF strives to present clear and unbiased information. This site is partially funded through a grant from Bayer Healthcare, LLC.

© Copyright 2000-2013 Multiple Sclerosis Foundation - All Rights Reserved

�