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Interferon Beta–Induced Restoration of Regulatory T-Cell Function in Multiple Sclerosis Is Prompted by an Increase in Newly Generated Naive Regulatory T Cells
Mirjam Korporal, MD;
Juergen Haas, PhD;
Bettina Balint;
Benedikt Fritzsching, MD;
Alexander Schwarz, MD;
Sigrid Moeller, MD;
Brigitte Fritz;
Elisabeth Suri-Payer, PhD;
Brigitte Wildemann, MD
Arch Neurol. 2008;65(11):1434-1439.
Background Naturally occurring regulatory T (Treg) cells are functionally impaired in patients with relapsing-remitting multiple sclerosis. We recently showed that prevalences of newly generated CD31-coexpressing naive Treg cells (recent thymic emigrant–Treg cells) are critical for suppressive function of circulating Treg cells, and a shift in the homeostatic composition of Treg-cell subsets related to a reduced de novo generation of recent thymic emigrant–Treg cells may contribute to the multiple sclerosis (MS)–related Treg-cell dysfunction. Interferon beta, an immunomodulatory agent with established efficacy in MS, lowers relapse rates and slows disease progression. Emerging evidence suggests that Treg-cell suppressive capacity may increase in patients with MS undergoing treatment with interferon beta, although the mechanisms mediating this effect are uncertain.
Objective To evaluate the effect of interferon beta treatment on the suppressive activity and the homeostasis of circulating Treg cells in patients with MS.
Participants Twenty patients with relapsing-remitting MS and 18 healthy control subjects.
Interventions Administration of interferon beta.
Main Outcome Measures Effect of interferon beta on Treg-cell homeostasis and suppressive capacity.
Results Suppressive capacities of Treg cells were consistently upregulated at 3 and 6 months after treatment with interferon beta. The restoration of Treg-cell function was paralleled by increased naive recent thymic emigrant–Treg cells and a coincidental reduction in memory Treg cells.
Conclusion The increase in Treg-cell inhibitory capacity mediated by interferon beta treatment can be explained by its effect on the homeostatic balance within the Treg cell compartment.
Author Affiliations: Division of Molecular Neuroimmunology, Department of Neurology (Drs Korporal, Haas, Schwarz, Moeller, and Wildemann and Mss Balint and Fritz), and Division of Neonatology, Children's Hospital (Dr Fritzsching), University of Heidelberg, and Division of Immunogenetics/Tumor Immunology Program, German Cancer Research Centre (Dr Suri-Payer), Heidelberg, Germany.
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Arch Neurol 2008;65:1417-1418.
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