ulusoy, canan istanbul university - institute for experimental medicine - department of neuroscience, Turkey , karaaslan, zerrin istanbul university - institute for experimental medicine - department of neuroscience, Turkey , özyurt, selen haydarpasa numune training and research hospital - department of neurology, Turkey , erdağ, ece istanbul university - institute for experimental medicine - department of neuroscience, Turkey , türkoğlu, recai haydarpasa numune training and research hospital - department of neurology, Turkey

NEURONAL SURFACE ANTIBODIES ARE NOT FOUND IN MULTİPLE SCLEROSIS PATIENTS WITH TUMEFACTIVE DEMYELINATING LESIONS

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Tumefactive demyelinating lesion (TDL) is a brain lesion with a diameter of 2 cm or more and is often associated with a mass effect, perilesional edema and ring enhancement. TDLs are occasionally encountered in multiple sclerosis (MS) and neuromyelitis optica (NMO) patients. To find out whether antibodies directed against aquaporin 4 (Aqp-4) and neuronal surface antigens (ion channels and other neuronal membrane proteins) are involved in TDL pathogenesis, we screened a panel of wellcharacterized anti-neuronal antibodies and neuronal cell surface antibodies in relapsing remitting MS cases presenting with TDLs.Seven relapsing remitting MS patient (6 women, 1 man; average agestandard deviation 42.2±11.7 year-old) presenting with neurological episodes characterized with TDLs, Controls included age/gender matched relapsing remitting MS patients without any history of TDLs (n=40), autoimmune limbic encephalitis and NMO patients with well-characterized antibodies (n=25) and healthy individuals (n=50). None of the MS patients with or without TDLs and healthy controls showed antibodies directed against wellcharacterized neuronal surface antigens or any other cell membrane antigen expressed by cultured live neuronal cells. By contrast, control autoimmune encephalitis and NMO patients showed various serum antineuronal antibodies (5 Aqp-4, 3 CASPR2, 3 LGI1, 5 NMDAR, 2 AMPAR, 2 GABABR, 5 GAD antibody positivity), as expected. Our study failed to reveal any association between TDL occurrence and neuronal surface antibodies. Our results imply that absence of serum anti-neuronal antibodies reacting with membrane antigens of cultured live neurons in TDL patients suggests that antibody-mediated mechanisms are not involved in TDL pathogenesis.

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Deneysel Tıp Araştırma Enstitüsü Dergisidir

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