A study published in the Journal of Immunology has confirmed that the cytokine granulocyte macrophage colony-stimulating factor (GM-CSF) likely plays a critical role in multiple sclerosis (MS) in humans, and has proposed a new reasoning for why treatment with interferon-beta is often effective in reducing MS attacks.
Th-17 cells became a new focus as it appeared to play a role in neuronal damage progression in MS. This led researchers to believe that cytokine IL-17, produced by Th-17 cells, was also important to MS.
However in 2011, researchers from Thomas Jefferson University found that Th-17 cells also produced cytokine GM-CSF, which reacted with another cell type, significantly increasing its levels in the brain of mouse models.
In addition, mice that were unable to produce GM-CSF never developed the disease, though mice lacking IL-17 did develop mild disease.
To assess whether the same observation was true in human disease, researchers tested blood samples of patients with MS who had not received treatment, those who were receiving interferon-beta, or normal subjects.
They found that patients who were untreated had two to three times as many immune cells producing GM-CSF as did patients being treated with interferon-beta or normal subjects.
The team also studied brain samples of deceased patients with MS and discovered increased numbers of GM-CSF-producing cells in comparison to normal brain samples.
Findings support that GM-CSF is an important target and researchers hope future treatments can better block the harmful immune reaction in the central nervous system for these patients.
This article originally appeared on MPR