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Multiple Sclerosis
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Article

Multiple sclerosis-associated retroviral agent (MSRV)-stimulated cytokine production in patients with relapsing-remitting multiple sclerosis

M Saresella1, A Rolland2, I Marventano1, R Cavarretta3, D Caputo3, P Marche2, H Perron4, and M Clerici5*

1 Laboratory of Molecular Medicine and Biotechnology, Don C. Gnocchi ONLUS Foundation IRCCS, Via Capecelatro, 66, Milano 20148, Italy
2 Laboratoire d'Immunochimie,CEA/INSERUM-U548, 17 rue des Martyrs 38054 Grenoble, France
3 Multiple Sclerosis Unit, Don C. Gnocchi ONLUS Foundation, IRCCS, Via Capecelatro, 66, Milano 20148, Italy
4 GeNeuro, Geneva; 1228 Plan-Lesouates, Switzerland
5 Laboratory of Molecular Medicine and Biotechnology, Don C. Gnocchi ONLUS Foundation IRCCS, Via Capecelatro, 66, Milano 20148, Italy; Chair of Immunology, Department of Biomedical Sciences and Technologies, University of Milano, Via Fratelli Cervi 93, Milano 20090, Italy

* To whom correspondence should be addressed.


  Abstract

Background

Human endogenous retroviruses are suggested to play a pathogenic role in multiple sclerosis (MS); one of such retroviruses, the MS-associated retroviral agent (MSRV) has repeatedly been isolated in MS patients.

Objective and methods

We analyzed cytokine profiles in MSRV envelope protein (MSRV ENV-SU)-stimulated peripheral blood mononuclear cells of 30 relapsing-remitting MS patients with either acute (AMS) (n = 13) or stable (SMS) (n = 17) disease. Results suggest that MSRV ENV-SU induces the production of inflammatory cytokines, including tumor necrosis factor-{alpha} (P < 0.05) and interferon-{gamma} (P < 0.004) in AMS patients and of interleukin-10 (P < 0.05), an inflammation-dampening cytokine, in SMS individuals.

Conclusions

These data strengthen the hypothesis indicating that MSRV could be involved in the pathogenesis of MS.

Key Words: cytokines, ENV-SU protein, human endogenous retroviruses (HERV), immunology, multiple sclerosis, T lymphocytes

First published on February 27, 2009, doi:10.1177/1352458508100840

Multiple Sclerosis 2009;15:443.

A more recent version of this article appeared on April 1, 2009

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