Dr. Aris from BioVista was kind enough to return my email where I asked for a layman’s description of MOG-induced Experimental Allergic Encephalomyelitis (EAE).

Although no animal model thus far establishes all facets of human MS, Experimental Allergic Encephalomyelitis (EAE) induced in rodents represents the model most studied for the disease. The origin of the model is traced to the development of the rabies vaccine. Encephalomyelopathy was caused in a small percentage of humans who received the rabies vaccine. Historically is has been thought that Th1 cells played a predominant role in the pathology of the disease. However, recent evidence suggests that a proinflammatory cascade of Th17 cells, IL-6 and TGF-b in the central nervous system plays a critical role in the pathogenesis of EAE and MS.
Initially rodent brain homogenates were used as antigens for immunization. Today, myelin related proteins or peptides are used for the induction of the disease. Among the most commonly employed are MBP (a major constituent of myelin), PLP (proteolipid protein only found in myelin) and MOG (myelin oligodendrocyte glycoprotein). Sections of PLP, such as 139-151, are encephalitogenic to certain mouse strains. The choice of the peptide together with the animal strain and way of induction will determine the type of disease one wants to mimic. MOG-induced EAE is a chronic disease and is the closest murine analog of Progressive Multiple Sclerosis.

Thank you Dr. Aris!