Abstract
Sulfatide is a major glycosphingolipid in myelin and a target for autoantibodies in autoimmune neuropathies. However neuropathy disease models have not been widely established, in part because currently available monoclonal antibodies to sulfatide may not represent the diversity of anti-sulfatide antibody binding patterns found in neuropathy patients. We sought to address this issue by generating and characterising a panel of new anti-sulfatide monoclonal antibodies. These antibodies have sulfatide reactivity distinct from existing antibodies in assays and in binding to peripheral nerve tissues and can be used to provide insights into the pathophysiological roles of anti-sulfatide antibodies in demyelinating neuropathies.
Highlights
Sulfoglycolipids are common components of the mammalian plasma membrane that are distinguished by the presence of a sulfate group
Combinatorial glycoarrays from serum taken at day 28 post immunisation indicated that IgM antibodies were generated to all membrane lipids comprised in the liposomes and their complexes; fluorescence intensity represents the binding signals (Fig. 1A)
All genotypes and strains studied generated anti-sulfatide IgM antibodies, which could be detected in their sera from 14 days post-immunisation (Fig. 1B)
Summary
Sulfoglycolipids are common components of the mammalian plasma membrane that are distinguished by the presence of a sulfate group. After 6 weeks, disorganisation of the myelin and disassembly of the nodes of Ranvier and paranodal junctions occurs, indicated by decreased Na+ and K+ channel clustering and abnormal distribution of K+ channels that are misplaced from the juxtaparanodes into the paranode (Hoshi et al, 2007; Ishibashi et al, 2002; Marcus et al, 2006; Takano et al, 2012). These disturbances directly correlate with sulfatide content in the peripheral nerve, as evidenced by combined biochemical and functional studies (Hayashi et al, 2013). The temporal and mechanistic sequence by which these demyelinating events evolve is not understood, in part owing to limited information on sulfatide distribution in glial cell membranes
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