![]() Demyelination was accompanied by increased microglia activation however, the morphology and survival of astrocytes, oligodendrocyte progenitors and neurons remained unaffected. Myelin-specific MS rAbs initiated complement-dependent cytotoxicity to oligodendrocytes and induced rapid demyelination. MS myelin-specific rAbs bound to discrete surface domains on oligodendrocyte processes and myelinating axons. ![]() Demyelination, glial and neuronal viability, and complement pathway activation were assayed by immunofluorescence microscopy and compared to the effects of an aquaporin-4 water channel (AQP4)-specific rAb derived from a neuromyelitis optica (NMO) patient. We examined their immunoreactivity to mouse organotypic cerebellar slices by live binding and evaluated tissue injury in the presence and absence of human complement. Among these were a subset of myelin-specific MS rAbs. We produced IgG1 monoclonal recombinant antibodies (rAbs) from clonally-expanded plasmablasts recovered from MS patient CSF. Both the specific targets and pathogenic effects of MS antibodies remain poorly characterized. Intrathecal immunoglobulin G (IgG) synthesis, cerebrospinal fluid (CSF) oligoclonal IgG bands and lesional IgG deposition are seminal features of multiple sclerosis (MS) disease pathology.
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