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Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis

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Interferon-beta increases BAFF levels in multiple sclerosis: implications for B cell autoimmunity.

M Krumbholz¹, H Faber, F Steinmeyer

¹Department of Neuroimmunology, Max Planck Institute of Neurobiology, Am Klopferspitz 18, 82152 Martinsried, Germany.

Brain : a Journal of Neurology

|May 14, 2008

Summary

This summary is machine-generated.

Interferon-beta therapy for multiple sclerosis increases BAFF, a B cell survival factor. This may explain why some patients respond less to treatment and could promote autoantibody production.

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Area of Science:

Immunology
Neuroimmunology
Pharmacology

Background:

B cells play a key role in multiple sclerosis (MS) pathogenesis.
The BAFF/APRIL system is vital for B cell survival and can drive autoimmune diseases.
Interferon-beta (IFN-beta) is a common treatment for MS.

Purpose of the Study:

To investigate the impact of IFN-beta therapy on the BAFF/APRIL system in MS patients.
To determine if IFN-beta influences BAFF and APRIL ligand and receptor expression.
To explore the relationship between BAFF levels and therapeutic response in MS.

Main Methods:

Analysis of BAFF, APRIL, and TWE-PRIL ligand and receptor transcription via TaqMan-PCR in blood cells from 107 MS patients.
Measurement of serum BAFF concentrations using ELISA.
In vitro induction of BAFF by IFN-beta in cultured immune and non-immune cells.

Main Results:

IFN-beta therapy significantly upregulated BAFF transcription in monocytes and granulocytes, correlating with the MxA biomarker.
Elevated serum BAFF levels were found in IFN-beta-treated MS patients, comparable to Systemic Lupus Erythematosus (SLE) patients.
IFN-beta induced BAFF in vitro at concentrations relevant to therapeutic levels; BAFF was the primary regulated component of the BAFF/APRIL system.

Conclusions:

IFN-beta therapy potently induces BAFF, a B cell survival factor, in MS patients.
This BAFF induction may contribute to autoantibody production and IFN-neutralizing antibodies.
The findings suggest that some MS patients, particularly those with significant B cell involvement, might benefit less from IFN-beta therapy due to BAFF upregulation, explaining inter-individual treatment response variability.