Last June NeuroImmunology attended the 2011 Biennial meeting of the Peripheral Nerve Society in the Bolger Center, Potomac (MD). We were obviously interested in disimmune disorders but, we must recognize that, probably, breakthrough, surprising and interesting works were outside our field. Genetic and acquired neuropathies sessions showed, in our oppinion, a higher level than disimmune neuropathies ones. However, the whole meeting was pretty interesting and some useful conclusions made us think that past work may be starting to give results. I have several comments and remarks regarding disimmune neuropathies: For me, the first and most important conclussion is the desperate need we have in knowing a lot more of disimmune neuropathies pathogenesis: Guillain-Barré syndrome studies are focused almost exclusively in antiganglioside antibodies (which, to date, are the best and more solid research line in these disorders) and don’t seem to point in any other direction, cause or mechanism. However, the ambitious GBS multicentric database projected by Dr Jacobs’ group will, for sure, help in performing other kind of studies, genetic, pathologic and immunopathogenic. We hope we can move on antiganglioside antibodies and see beyond. Dr Huizinga, from Dr Jacobs group, presented their job on dendrictic cell role in GBS pathogenesis and molecules implicated in dendritic cell priming of B cells. It seems that new, non-antiganglioside, works are arising. Regarding antiganglioside antibodies, all posters presented by Dr Willison and Yuki groups were also remarkable. CIDP is, by far, the less known of all disimmune neuropathies. We still debate if auto-antibodies or T cells are the effectors. Immunopathogenic studies are scarce, weak and based in imperfect models (modified from multiple sclerosis ones, like experimental autoimmune neuritis – EAN- ). The most remarkable work in CIDP and related diseases was presentation by Gerd Meyer zu Horste, from Dr Kieseier’s lab, showing a new
AAN evidence based reviews don’t add anything new to what we probably know (or should know) or suspect about a treatment or intervention, but it’s always useful to have all data summarized to avoid the whole process of revision by oneself. In the last issue of Neurology journal we’ll find an evidence-based review about the use of plasmapheresis in neurological disorders. Not any surprise in GBS and CIDP being the diseases with a better level of evidence in plasmapheresis efficacy. Not anything to question, but just highlight a (small) paradox… One of the main mechanisms of action of plasmapheresis is pathogenic antibody removal, then, how can a well known antibody mediated disease like myasthenia have less evidence than those diseases in which cellular immunity is considered more important, such as MS or CIDP?