PT  - JOURNAL ARTICLE
AU  - Anne I. Boullerne
AU  - José J. Rodrı́guez
AU  - Tarik Touil
AU  - Bruno Brochet
AU  - Stephan Schmidt
AU  - Nora D. Abrous
AU  - Michel Le Moal
AU  - Jeffrey R. Pua
AU  - Mark A. Jensen
AU  - Willy Mayo
AU  - Barry G. W. Arnason
AU  - Klaus G. Petry
TI  - Anti-<em>S</em>-Nitrosocysteine Antibodies Are a Predictive Marker for Demyelination in Experimental Autoimmune Encephalomyelitis: Implications for Multiple Sclerosis
AID  - 10.1523/JNEUROSCI.22-01-00123.2002
DP  - 2002 Jan 01
TA  - The Journal of Neuroscience
PG  - 123--132
VI  - 22
IP  - 1
4099  - http://www.jneurosci.org/content/22/1/123.short
4100  - http://www.jneurosci.org/content/22/1/123.full
SO  - J. Neurosci.2002 Jan 01; 22
AB  - Multiple sclerosis (MS) is characterized by inflammation within the CNS. This inflammatory response is associated with production of nitric oxide (NO) and NO-related species that nitrosylate thiols. We postulated that MS patients would exhibit an antibody (Ab) response directed against proteins containing S-nitrosocysteine (SNO-cysteine) and showed that anti-NO-cysteine Abs of the IgM isotype are in fact present in the sera of some MS patients (Boullerne et al., 1995). We report here the presence of a seemingly identical Ab response directed against SNO-cysteine in an acute model of MS, experimental autoimmune encephalomyelitis (EAE) induced in Lewis rats with the 68–84 peptide of guinea pig myelin basic protein (MBP68–84). Serum levels of anti-SNO-cysteine Abs peaked 1 week before the onset of clinical signs and well before the appearance of anti-MBP68–84 Abs. The anti-SNO-cysteine Ab peak titer correlated with the extent of subsequent CNS demyelination, suggesting a link between Ab level and CNS lesion formation. In relapsing–remitting MS patients, we found elevated anti-SNO-cysteine Ab at times of relapse and normal values in most patients judged to be in remission. Two-thirds of patients with secondary progressive MS had elevated anti-SNO-cysteine Ab levels, including those receiving interferon β-1b. The data show that a rise in circulating anti-SNO-cysteine Ab levels precedes onset of EAE. Anti-SNO-cysteine Abs are also elevated at times of MS attacks and in progressive disease, suggesting a possible role for these Abs, measurable in blood, as a biological marker for clinical activity.