Diseases experimental allergic encephalomyelitis

In autoimmunity models, similar interactions occur. Thus, mice exposed to S. mansoni ova are protected from two different autoimmune diseases, type 1 diabetes [71] and experimental allergic encephalomyelitis [72, 73]. In these instances, a Th2 immune deviation might equally explain the amelioration of Thl pathology, and experimental testing of this possibility remains to be undertaken. 

Multiple sclerosis (MS) has traditionally been viewed as a disorder in which myelin is the primary target. However, there is recent evidence for abnormal SNS expression in experimental models of demyelination and in MS. Black et al (1999b) studied Na channel expression in the taiep rat, a mutant model in which myelin is initially formed normally, but then lost as a result of an oligodendrocyte abnormality. They observed the abnormal expression of SNS Na channel mRNA and protein in Purkinje cells following loss of myelin. More recently. Black et al (2000) demonstrated that SNS mRNA and protein, which are not detectable in normal Purkinje cells, are expressed within Purkinje cells in a mouse model of MS, chronic relapsing experimental allergic encephalomyelitis. Black et al (2000) have also demonstrated the expression of SNS mRNA (Fig. 7a, b) and protein (Fig. 7e, f) within cerebellar Purkinje cells from tissue obtained post-mortem from MS patients, but not in controls with no neurological disease (Fig. 7c, g). 

In induced models, a susceptible animal strain is immunized with a mixture of an adjuvant and an autoantigen isolated from the target organ. Examples are adjuvant arthritis in the Lewis strain rat (Pearson, 1956) and experimental allergic encephalomyelitis, a model of multiple sclerosis (Ben-Nun Cohen, 1982). Induced models are often used to study the pathogenesis of and therapeutic venues for relevant autoimmune diseases. These models have been proposed as means to evaluate the immunomodulatory effects of chemicals on ongoing autoimmune diseases in a second tier of immunotoxicity testing. 

Experimental allergic encephalomyelitis (EAE). Autoimmune demyelinating disease induced in genetically susceptible mice, rats, or marmosets by immunization with myelin proteins or peptides. Animal model for multiple sclerosis. 

Pelletier L, Rossert J, Pasquier R, Villarroya H, Belair MF, Vial MC, Oriol R, Druet P (1988) Effect of HgCb on experimental allergic encephalomyelitis in Lewis rats. HgCb-induced down-modulation of the disease. Eur J Immunol, 18(2) 243-247. 

M. B. Tanzola et al., Mast cells exert effects outside the central nervous system to influence experimental allergic encephalomyelitis disease course, Journal of Immunology, 171, 2003, 4385-91. 

The MBPS are a family of proteins. Unlike PLP, MBPs are easily extracted from the membrane and are soluble in aqueous solution. The major MBP has no tertiary structure and has a molecular weight of 15,000 Daltons. MBP is located on the cytoplasmic face of myelin membranes. Antibodies directed against MBPs elicit experimental allergic encephalomyelitis (EAE), which has become a model system for understanding multiple sclerosis, a demyelinating disease. A model of how PLP and MBPs aid in stabilizing myelin is shown in Figure 48.14. 

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