Next Article in Journal
Erythropoietin (EPO) as a Key Regulator of Erythropoiesis, Bone Remodeling and Endothelial Transdifferentiation of Multipotent Mesenchymal Stem Cells (MSCs): Implications in Regenerative Medicine
Next Article in Special Issue
Signaling through the S1P−S1PR Axis in the Gut, the Immune and the Central Nervous System in Multiple Sclerosis: Implication for Pathogenesis and Treatment
Previous Article in Journal
Mechanisms of Smoothened Regulation in Hedgehog Signaling
Previous Article in Special Issue
Extracellular Vesicles in Multiple Sclerosis: Role in the Pathogenesis and Potential Usefulness as Biomarkers and Therapeutic Tools
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Cells
Volume 10
Issue 8
10.3390/cells10082139
Review Report
cells-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles
Article
Peer-Review Record

Interferon-β Intensifies Interleukin-23-Driven Pathogenicity of T Helper Cells in Neuroinflammatory Disease

Cells 2021, 10(8), 2139; https://doi.org/10.3390/cells10082139
by Agnieshka Agasing, James L. Quinn, Gaurav Kumar and Robert C. Axtell *
Reviewer 2: Anonymous
Cells 2021, 10(8), 2139; https://doi.org/10.3390/cells10082139
Submission received: 10 July 2021 / Revised: 18 August 2021 / Accepted: 19 August 2021 / Published: 20 August 2021
(This article belongs to the Special Issue Cellular and Molecular Mechanisms of Multiple Sclerosis Pathogenesis)

Round 1

Reviewer 1 Report

1) Please, replace "yet" for "however".

2) Do the authors claim that IFN-beta exacerbates neuroinflammation? What about the treatment of patients with RRMS who receive this medication?

Author Response

We thank the reviewer for the constructive comments.  They have been addressed below and changes are highlighted in the manuscript.

Comment 1: “Please, replace "yet" for "however".”   

  • We have changed each “yet” to “however”.

Comment 2: “Do the authors claim that IFN-beta exacerbates neuroinflammation? What about the treatment of patients with RRMS who receive this medication?”

  • Our previous publications and work from other research groups have shown that patients with high levels of TH17 signatures, which include a subset of MS patients and NMO patients, are non-responders to IFN-beta therapy and this therapy may increase disease. In these studies, we have also identified that markers in the TH1 pathway are indicative of a good response to IFN-beta therapy in MS.
  • This current manuscript provides further mechanisms on how IFN-beta can drive disease activity in NMO and in subsets of IFN-non responder MS patients.
  • We have clarified this in the introduction of the manuscript.  

Reviewer 2 Report

This is an experimental trial which points out some still unknown MoA of Interferon. Concening the introduction I would recommend that the authors discuss missing compliance of MS patients as further cause for the relatively high rate of patients, who do not respond to interferon therapy in MS. There are data from Germany, who describe this due to the high side effect potential of  interferons with flu-like symptoms. The authors may discuss whether this behaviour may contribute to rebound phenomena as a cause for relapses simlar to fingolimod. May this cytokine regulation via interferons may trigger relapses as rebound phenomena in MS ?  

 

Author Response

We thank the reviewer for pointing out that therapeutic compliance may contribute to non-responsiveness to IFN-beta in some patients. We now have mentioned and cite three possibilities for non-response to therapy in the introduction of the manuscript: Non-compliance, neutralizing antibodies, and immunological signatures.   

Round 2

Reviewer 2 Report

it is okay now

Author Response

Thank you.

Back to TopTop