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Related Experiment Video

Updated: Jul 5, 2026

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

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Published on: March 24, 2015

Increased IL-10 mRNA and IL-23 mRNA expression in multiple sclerosis: interferon-beta treatment increases IL-10 mRNA

M Krakauer¹, P Sorensen, M Khademi

¹Danish Multiple Sclerosis Research Center, Department of Neurology, Copenhagen University Hospital, Rigshospitalet Copenhagen, Denmark. martin.krakauer@dadlnet.dk

Multiple Sclerosis (Houndmills, Basingstoke, England)

|April 22, 2008

Summary

Interferon-beta therapy for multiple sclerosis (MS) does not shift Th1/Th2 cytokines but increases regulatory IL-10 and decreases IL-23, potentially impacting the Th17 axis.

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Published on: May 8, 2016

Area of Science:

Immunology
Neuroimmunology
Molecular Biology

Background:

Multiple sclerosis (MS) treatment with Interferon-beta (IFN-beta) is controversial regarding its proposed shift from pathogenic Th1 to less detrimental Th2 cytokines.
Investigating in vivo cytokine and transcription factor mRNA expression in blood mononuclear cells (MNCs) and whole blood during IFN-beta therapy in MS patients is crucial.

Purpose of the Study:

To analyze the in vivo effects of IFN-beta therapy on cytokine and transcription factor mRNA expression in patients with multiple sclerosis.
To determine if IFN-beta therapy promotes a Th1 or Th2 cytokine profile shift in MS patients.

Main Methods:

Real-time reverse transcriptase polymerase chain reaction (PCR) was used to analyze mRNA expression.
Blood samples were collected from 20 relapsing-remitting MS patients before and after 3 months of IFN-beta treatment.
Findings were confirmed in an additional cohort of 39 MS patients and 50 healthy volunteers.

Main Results:

Untreated MS patients exhibited elevated levels of interleukin (IL)-23 and IL-10 mRNA.
IFN-beta therapy led to increased IL-10 and decreased IL-23 mRNA expression, independent of Th1 or Th2 cytokines.
The most significant changes in cytokine mRNA levels were observed early after IFN-beta injection (approximately 9-12 hours).

Conclusions:

IFN-beta therapy in MS does not appear to promote a Th1 or Th2 mRNA expression profile.
The therapeutic benefits of IFN-beta are likely mediated by the induction of the regulatory cytokine IL-10.
Decreased IL-23 mRNA levels following IFN-beta therapy suggest the Th17 axis, implicated in MS pathogenesis, may also be a therapeutic target.