- Meeting abstract
- Open Access
Innate and adaptive anti-viral immune responses in MS patients treated with interferon-beta
© Petersen et al; licensee BioMed Central Ltd. 2011
- Published: 6 June 2011
- Multiple Sclerosis
- Multiple Sclerosis Patient
- Complement Activation
- Adaptive Immune Response
- Antiviral Response
Interferon-beta (IFN-β) has both immuno-modulating and anti-viral effects. In a longitudinal study of multiple sclerosis (MS) patients undergoing interferon-beta therapy, we have performed a comprehensive study of factors in the innate and adaptive immune response to the two types of virus associated with MS: human endogenous retroviruses (HERVs), and herpesviruses.
Anti-viral antibodies towards HERVs and herpesviruses were assayed using TRIFMA or ELISA. Cytokine profiling was performed using the Luminex-system. Factors in the lectin complement activation pathway were assayed using TRIFMA.
We demonstrate significant decreases in anti-Envelope antibody reactivity for the two closely related Gammaretroviral HERVs, HERV-H and HERV-W, as a consequence of IFN-β therapy, closely linked to efficacy of therapy/low disease activity. We also found strong indications of a protective effect of high levels of two components in the innate pathogen-associated molecular pattern recognition: mannan-binding lectin (MBL), and MASP-3.
Serum levels of typical Th1- and Th2- related, MS-relevant cytokines were also monitored. We found no overall changes in Th1/Th2 ratios.
Our results support that IFN-β exerts effects on immune response to HERV-H/HERV-W, and that this antiviral response may play a role in MS development. Components in the immune response to HERVs have potential as biomarkers for disease activity.
This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.