Modelling paraneoplastic CNS disease: T-cells specific for the onconeuronal antigen PNMA1 mediate autoimmune encephalomyelitis in the rat.

Antibodies directed against onconeuronal antigens provide a specific diagnostic marker for paraneoplastic neurological syndromes (PNS) and suggest that these autoantigens are targeted during disease pathogenesis. However, so far attempts to generate autoimmune models of PNS have been unsuccessful. Here we show that the adoptive transfer of T-cells specific for the autologous onconeuronal antigen Pnma1 cause encephalomyelitis in the Dark Agouti (DA) rat.

Myelin oligodendrocyte glycoprotein is expressed in the peripheral nervous system of rodents and primates.

The myelin oligodendrocyte glycoprotein (MOG) is a minor CNS myelin-specific protein that is an important candidate autoantigen in multiple sclerosis. We now report that MOG mRNA transcripts are present in the peripheral nervous system of rodents and primates at levels approximately ten-fold lower than in brain as demonstrated by real time PCR. A major source of this signal are Schwann cells which are also shown to express MOG protein within their cytoplasm in vitro by immunohistochemistry.

Genetic variation in myelin oligodendrocyte glycoprotein expression and susceptibility to experimental autoimmune encephalomyelitis.

Myelin oligodendrocyte glycoprotein (MOG) is encoded within the RT1.M region of the rat MHC a susceptibility locus for MOG-induced experimental autoimmune encephalomyelitis (EAE). We report that the enhanced susceptibility of Brown Norway (BN) rats to MOG-EAE is associated with higher expression of MOG mRNA and protein in the nervous system than in the less susceptible Lewis (LEW) strain.

Myelin oligodendrocyte glycoprotein-specific T cell receptor transgenic mice develop spontaneous autoimmune optic neuritis.

Multiple sclerosis (MS) is considered to be an autoimmune disease of the central nervous system (CNS) that in many patients first presents clinically as optic neuritis. The relationship of optic neuritis to MS is not well understood. We have generated novel T cell receptor (TCR) transgenic mice specific for myelin oligodendrocyte glycoprotein (MOG).