SERUM AUTOANTIBODIES IN PATIENTS WITH RELAPSING REMITTING MULTIPLE SCLEROSIS (RRMS)

PEREIRA BRUNELLI MC ; ADELINA B, ; MARTINEZ A; CORREALE J; RAMOS AJ

Congreso; Reunion Anual de la Sociedad Argentina de Investigación Clínica; 2018

Multiple sclerosis is a chronic inflammatory disease of the CNS that manifests as acute focal inflammatory demyelination and axonal loss with limited remyelination. The activated T lymphocyte, with receptors for components of the CNS myelin, crosses the blood-brain barrier and responds locally to its target antigen, triggering the inflammatory cascade. The antibodies produced during inflammation can be found in peripheral blood and assessed by different methods. The detection of the antibodies was carried out by indirect immunofluorescence from in vitro cell culture of astrocytes and oligodendrocytes, indirect immunofluorescence from prepared with rat cerebellum slices and immunoblot assays from rat cerebellum extract. A total of 99 samples were analyzed, 64 from patients with a diagnosis of RR MS (Group 1) and 35 without diagnosis of disease (Group 2). Both groups analyzed with in vitro cell culture of astrocytes and oligodendrocytes were non-reactive. By the prepared with rat cerebellum slices, group 1 showed reactivity in 84.4% of the samples (3.1% in 1/10 dilution and 81.3% in 1/40 dilution) against the white sheet with different fluorescence patterns (homogeneous 26,6%, homogeneous granular fine 21,9%, homogeneous granular thickness 35,9%) and group 2 no reactivity was observed. In the immunoblot assays, bands were observed at the molecular weight level corresponding to the proteins of the myelin band in samples that were reactive by indirect immunofluorescence. The autoantibodies produced during inflammation are directed against the myelin band and mature oligodendrocytes, also depending on the type of treatment of each patient can be detected by indirect immunofluorescence. The different fluorescence patterns observed could be due to reasons such as not all patients produce the same autoantibodies during inflammation.