Mice are back in the frame as MOG T cell reactivity in MS is higher than first thought


Myelin oligodendrocytes glycoprotein is a CNS specific protein on the surface of myelin. Therefore it can be attacked by antibodies and this can cause demyelination in beasties. Disease induction in EAE was first shown by Dr Love in 1994. A little later it was shown that a Myelin oligodendrocyte protein peptide could induce disease in C57BL/6 mice on which transgenics and gene knockout mice were made. So it became the new potential autoantigen for MS. Trouble was that only a few people with MS appeared to respond to it. A T cell receptor transgenic mouse was made and it got optic neuritis and spinal cord disease and they called it Devics Mice. Essentially all rodent EAE is largely spinal cord driven with little brain involvmenet so Devics mouse wasn’t appropriate. However Devic’s MS which is associated with optic nerve and spinal cord involvement became neuromyelitis opitca (NMO) and this wasn’t MS. It was first found that antibodies to a water channel were important. However then a MOG-spectrum disorder was found and abit like NMO. In humans NMO has neutrophils and as mouse EAE has neurophils, EAE appeared to become an NMO model. However, this new study claws EAE back because using a more sensitive Test it wasn’t 10% that reposond to MOG it is present in about 50% of people with MS. Is this the cause of MS, or a consequnce of MS/

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  • Mmmm. So, what does this mean for patients that are AQ4P negative but MOG positive and have an NMOSD diagnosis? This raises serious questions around treatment.

  • Stop fluffing around and going round in a circles. Migrate to cloud on Azure. Load all the articles to data lake using data bricks. Nosql databases required or formatting required. Turn on Machine learning. Watch how algorythm infer links that u havnt even considered. Granted some patterns maybe a coincidence.



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