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 model of CIDP obtained knocking out ICAM-1 in NOD mice. Apart from this job, Dr Kieseier’s group is the only one that consistently publishes in CIDP basic immunology, and that was evident in the number of presentations in the meeting. In the same direction of disease models, Dr Figlia, from Angelo Quattrini group presented a beautiful conference about a model of demyelinating neuropathy caused in mice by an spontaneous mutation on dystroglycan. Although pathological features resembled those of a CIDP it pops up the question if that would fit better with an inherited cause of neuropathy, taking in account that dystroglycan is a necessary element of the extracellular matrix and has nothing to do with immune system (as far as i know). Anyway, beautiful work. Neurofascin was proposed by Dr Pollard group, as a novel antigen for GBS and CIDP. However, antigens detected by ELISA always raise the question if those antigens, detected in their denaturalized situation would be detected as well in conformational, natural situations and, thus, could be pathogenic. But, again, nice stuff to work on.
  • Nothing remarkably new was presented in multifocal motor neuropathy and paraproteinemic neuropathies pathogenesis. In anti-MAG neuropathy i liked a work, by an Argentinian group (Dr Lopez and co-workers) on the protective role of MAG for motor neurons.

The other main conclusion i reached in the meeting was that the former (knowing better the mechanisms) should lead to better, more specific therapies. We are blindly trying whatever is being tested succesfully in other diseases and still have not any alternative therapy likely to become a standard treatment in the future, IVIG and steroids aside. We’ve tried Rituximab, Alemtuzumab, Natalizumab… but except the isolated case in which Natalizumab was used, nothing specifically chosen on an immunopathogenic basis. We still are eagerly waiting for a trial with Eculizumab in GBS

However, among all the IVIg and Rituximab noise, i found an interesting poster regarding therapy. A trial in rats comparing efficacy of a recombinant IgG-Fc compound that could substitute the scarce and expensive IVIg courses. It demonstrated to be as effective as conventional IVIg in EAN Lewis rats. We hope this could be the first step to a novel therapy that could avoid the need of donors that we have now with conventional IVIg.

In conclusion, although several good presentations were worth the trip, we got home the idea that more knowledge of mechanisms and more lab work is desperately needed to move forward in disimmune neuropathies. Unless we prefer to stay stuck to decades-old theories and treatments.

All the abstracts of the meeting can be found online here

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