Title:Characterization of Regulatory T-Cells in Multiple Sclerosis Patients Treated with Interferon Beta-1a
VOLUME: 17 ISSUE: 2
Author(s):Mohsen Ebrahimimonfared, Ali Ganji, Sara Zahedi, Parisa Nourbakhsh, Keyvan Ghasami and Ghasem Mosayebi*
Affiliation:Department of Neurology, School of Medicine, Arak University of Medical Sciences, Arak, Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Department of Hematology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak, Department of Neurology, School of Medicine, Arak University of Medical Sciences, Arak, Molecular and Medicine Research Center, Arak University of Medical Sciences, Arak
Keywords:Interferon beta-1a, multiple sclerosis, regulatory T-cells, myelin, sheath, CNS, Treg cells.
Abstract:Background: Regulatory T-Cells (Treg Cells), as one of the immune system components,
have been highly effective in the autoimmune diseases prevention, particularly multiple sclerosis
(MS). Cytokine-based therapies such as interferon beta-1a (IFN-β1a) is a common drug in MS treatment;
however, its exact mechanisms are insufficiently described.
Objective: Therefore, the goal of this study was to evaluate the in vivo impact of IFN-β1a on the Treg
Cells in MS.
Methods: In this case-control study, Treg Cells were analysed by flowcytometry in IFN-β1a-treated
relapsing-remitting MS (RRMS) in comparison with new cases of MS and healthy subjects.
Results: The frequency of Treg Cells in the IFN-β1a treated-RRMS was increased compared to the
new MS cases (P < 0.05). Furthermore, the MFIs of the CD4 and CD25 in T-Cells were significantly
reduced in new cases of MS and IFN-β1a-treated RRMS than the control subjects (P < 0.05). Additionally,
the FoxP3 MFIs in CD4 + CD25 + T-Cells of IFN-β1a-treated RRMS were significantly
lower than the new cases of MS.
Conclusion: Overall, the present study indicated that IFN-β1a as an immunomodulatory drug led to an
enhancement in Treg Cells population without CD4, CD25, and FoxP3 molecules upregulation in Treg
Cells.