Cerebrospinal fluid immunoglobulin G promotes oligodendrocyte progenitor cell migration

  title={Cerebrospinal fluid immunoglobulin G promotes oligodendrocyte progenitor cell migration},
  author={Seema K. Tiwari-Woodruff and Lawrence W. Myers and Jeff M Bronstein},
  journal={Journal of Neuroscience Research},
Multiple sclerosis (MS) is characterized by demyelination of the CNS with associated neurological deficits. Remyelination can occur but is often incomplete. The process of myelin repair requires the proliferation and migration of oligodendrocyte progenitor cells (OPC) into the lesion from the neighboring areas. OPC migration is altered by several factors, including antibodies that bind to OPC surface proteins. We have previously reported elevated anti‐OSP/claudin‐11 antibodies in the… 

The antibody response to oligodendrocyte specific protein in multiple sclerosis



T and B cell responses to myelin-oligodendrocyte glycoprotein in multiple sclerosis.

It is suggested that the myelin-oligodendrocyte glycoprotein may represent a pathogenetically important target Ag in multiple sclerosis.

Patients with active relapsing‐remitting multiple sclerosis synthesize antibodies recognizing oligodendrocyte progenitor cell surface protein: Implications for remyelination

In myelinating cultures, cell lysis with antibody recognizing a progenitor cell–specific surface glycoprotein (AN2) suppressed the synthesis of myelin proteins and contributed to the development and progression of chronically demyelinated lesions.

Human monoclonal antibodies reactive to oligodendrocytes promote remyelination in a model of multiple sclerosis.

The results are consistent with the hypothesis that CNS-reactive mAbs, part of the normal Ig repertoire in humans, may help repair and protect the CNS from pathogenic immune injury, and further challenge the premise that Abs that bind OLs are necessarily pathogenic.

T‐cell responses to oligodendrocyte‐specific protein in multiple sclerosis

It is demonstrated that OSP‐reactive T cells are part of the normal immune repertoire and therefore have the potential to contribute to the pathogenesis of MS.

Remyelination by Oligodendrocytes Stimulated by Antiserum to Spinal Cord

There is a factor present in anti-SCH antiserum that stimulates central nervous system-type remyelination and this finding may provide clues for the therapy of patients with demyelinating disorders such as multiple sclerosis.

Human antibodies accelerate the rate of remyelination following lysolecithin‐induced demyelination in mice

This study demonstrates that systemic administration of either polyclonal human immunoglobulins or specific human monoclonal antibodies can accelerate the rate of CNS remyelination following toxin‐induced demyelinated lesions, and proposes the use of humanpolyclonal IgM or specifichuman monoconal IgM antibodies as potential therapies to enhance myelin repair following CNS injury and disease.

A humoral response to oligodendrocyte-specific protein in MS

There is a specific humoral response directed against a region of OSP in RRMS patients that cross-reacts with several common viral peptides, which suggests a possible role for molecular mimicry in the development of MS.

Monoclonal autoantibody SCH94.03, which promotes central nervous system remyelination, recognizes an antigen on the surface of oligodendrocytes

Results raise the possibility that this monoclonal antibody SCH94.03 recognizes a novel oligodendrocyte‐specific surface antigen, and may act directly on oligodendedrocytes to promote remyelination.

Antibody facilitation of multiple sclerosis-like lesions in a nonhuman primate.

It is shown that the MS-like lesion can be reproduced by immunization against the extracellular domain of a single myelin protein, myelin/oligodendrocyte glycoprotein (MOG), which should facilitate development of specific immunotherapies for human MS.