This is an interesting new study that shows a certain antibody is present in MS'ers that attacks oligodendrocytes (say that 10 times in a row!). The oligo's are responsible for creating myelin, so killing these off prevents remyelination. Remylenation would of course be a holy grail for treating MS. The conclusion we draw from this article is that if you could stop these antibodies, you would allow the oligo's a much better chance at repairing damage to myelin. Now how to stop these antibodies... is there a molecular biologist in the house??

"Oligodendrocyte precursor cells (OPCs) are extremely efficient at remyelination. These cells persist in the adult human central nervous system and can proliferate. However, the failure to remyelinate is a pathological characteristic of the human demyelinating disease multiple sclerosis (MS), which suggests that these cells are ineffective in this disorder. This paper reports that IgG antibodies in the cerebrospinal fluid (CSF) of MS patients specifically recognize an antigen on OPCs in culture. Control patients were found not to possess these antibodies...

These results suggest that OPCs may be a target of anti-Hsp90 antibodies in MS patients and that this could prevent remyelination."

This is a PubMed entry, so it is a bit dense, but a wortwhile read-- click "read more" if you're up for the challenge.

Antibodies reactive to heat shock protein 90 induce oligodendrocyte precursor cell death in culture. Implications for demyelination in multiple sclerosis.

Cid C, Alvarez-Cermeno JC, Camafeita E, Salinas M, Alcazar A.

Servicio Bioquimica-Investigacion Hospital Ramon y Cajal, Madrid, Spain.

Oligodendrocyte precursor cells (OPCs) are extremely efficient at remyelination. These cells persist in the adult human central nervous system and can proliferate. However, the failure to remyelinate is a pathological characteristic of the human demyelinating disease multiple sclerosis (MS), which suggests that these cells are ineffective in this disorder. This paper reports that IgG antibodies in the cerebrospinal fluid (CSF) of MS patients specifically recognize an antigen on OPCs in culture. Control patients were found not to possess these antibodies. The antigen was immunoprecipitated in cell extracts from cultures with purified IgG from MS CSF. Peptide mass fingerprinting identified it as the beta type of heat shock protein 90 (Hsp90). Two-dimensional electrophoresis and immunoblot showed that this antigen in fact corresponds to two specific isoforms of Hsp90beta. Several control assays using monoclonal and polyclonal anti-Hsp90 antibodies confirmed the specific expression of Hsp90 on OPCs. Labeling OPCs in vivo with MS CSF and anti-Hsp90 antibodies and subsequent immunofluorescence confocal microscopy located the antigen on the cell surface. The binding of CSF antibodies from MS patients to the OPC surface led to complement activation and significant extinction of the OPC population. These results suggest that OPCs may be a target of anti-Hsp90 antibodies in MS patients and that this could prevent remyelination.

PMID: 14688203 [PubMed - in process]