A myelin-associated neurite outgrowth inhibitor Nogo-A plays a key role in inhibition of axonal regeneration. Axonal damage beginning at the early stage of multiple sclerosis (MS) is responsible for permanent neurological deficits, although its molecular mechanism remains unknown. The aim was to study the prevalence of autoantibodies against Nogo-A and Nogo receptor (NgR) in the serum of MS.Methods –
The antibodies were identified in the serum of 30 MS patients, 22 patients with non-MS other neurological diseases (OND), and 22 healthy control (HC) subjects by Western blot using recombinant human Nogo-A-specific segment (NAS), the shared segment of Nogo-A and -B (NAB), Nogo-66 (N66), the non-glycosylated form of NgR, the glycosylated NgR (NgR-Fc), and myelin oligodendrocyte glycoprotein (MOG).Results –
None showed immunoglobulin G (IgG) antibodies against NAS or NAB. In contrast, 30% of MS, 23% of OND and 32% of HC subjects exhibited anti-N66 IgG, while 27% of MS, 27% of OND and 18% of HC showed anti-MOG IgG. None of HC but 33% of MS and 14% of OND showed anti-non-glycosylated NgR IgG. Furthermore, 60% of MS, 18% of OND and 14% of HC showed anti-NgR-Fc IgG.Conclusions –
Because IgG autoantibodies against N66, NgR and MOG are often detected in the serum of MS and controls, they do not serve as an MS-specific marker.