Experimental allergic

Use of D-amino acids in the synthesis of a hairpin loop portion from the CD4 receptor provides a stable CD4 receptor mimic, which blocks experimental allergic encephalomyelitis (144). This synthetic constmct is not simply the mirror image or enantiomer of the CD4 hairpin loop, but rather an aH-D-constmct in the reverse sequence, thus providing stereochemicaHy similar side-chain projections of the now inverted backbone (Fig. 11). This peptide mimetic, unlike its aH-L amino acid counterpart, is resistant to en2yme degradation. As one would expect, the aH-D amino acid CD4 hairpin loop, synthesi2ed in the natural direction, the enantiomer of the natural constmct, is inactive. 

Rao, N.A., Wacker, W.B. and Marak, G.E. (1979). Experimental allergic uveitis clinicopathologic features associated with varying doses of S antigen. Arch. Ophthalmol. 97, 1954-1960. 

The genes of the inducible and the constitutively expressed forms of NOS have been cloned and expressed. The expression of inducible NOS in the brain tissue of animals with experimentally induced neurological disorders (boma disease virus and rabies virus in rats), herpes simplex virus (mice) and experimental allergic encephalitis (in rats) suggests that NO produced by induced NOS may be a toxic fector in the pathogenesis of neurological diseases (Koprowski et /., 1993). 

Benveniste EN. Role of macrophages/microglia in multiple sclerosis and experimental allergic encephalomyelitis. J Mol Med 1997 75 165-173. 

Raine, C. S., Wisniewski, H. and Prineas, J. An ultrastruc-tural study of experimental demyelination and remyelin-ation. II. Chronic experimental allergic encephalomyelitis in the peripheral nervous system. Lab. Invest. 21 316-327, 1969. 

P2 protein. PNS myelin contains a positively charged protein different from MBP that is referred to as P2 (Mr — 15,000). It is unrelated in sequence to MBP and is a member of a family of cytoplasmic fatty acid binding proteins (FABP) that are present in a variety of cell types [25]. The amount of P2 protein is variable among species, accounting for about 15% of total protein in bovine PNS myelin, 5% in humans and less than 1% in rodents. P2 protein is generally considered a PNS myelin protein but it is expressed in small amounts in CNS myelin sheaths of some species. P2 is an antigen for experimental allergic neuritis, the PNS counterpart of EAE (see Chs 36 and 38). P2 appears to be present in the major dense line of myelin sheaths, where it may play a structural role similar to MBP... 

Rouleau, A., Dimitriadou,V.,TrungTuong,M. D. etal. Mast cell specific proteases in rat brain changes in rats with experimental allergic encephalomyelitis. /. Neural Transm. 104 399-417,1997. 

Saida, T., Saida, K., Silberberg, D. H. and Brown, M. J. Experimental allergic neuritis induced by galactocerebro-side. Ann. Neurol. 9(Suppl.) 87-101,1981. 

Experimental allergic encephalomyelitis is an animal model of autoimmune demyelination 640... 

EAN experimental allergic neuritis GnRH gonadotropin-releasing hormone... 

Scelsi, R., D.M. Franciotta, C. Camana, F. Savoldi, and M. Allegrini. 1989. Suppression of experimental allergic encephalomyelitis after dietary zinc deprivation in guinea pigs. Nutr. Res. 9 1345-1354. 

Genetically predisposed animals or induced animal models may also be used to study and predict chemical-induced autoimmunity. 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 (AA), experimental allergic encephalomyelitis (EAE) and experimental uveitis in the Lewis strain rat. Examples of spontaneous models... 

Doganci A, Eigenbrod T, Krug N, et al Pathological role of IL-6 in the experimental allergic bronchial asthma in mice. Clin Rev Allergy Immunol 2005 28 257-270. 

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. 

Hachem PM, Lisbonne M, Michel L, Diem S, Roongapinun S, Lefort J, Marchal G, Herbelin A, Askenase PW, Dy M, Leite-de-Moraes MC a-Galactosylceramide-induced iNKT cells suppress experimental allergic asthma in sensitized mice role of IFN-7. Eur J Immunol 2005 35 2793-2802. 

Kleinjan A, Willart M, van Rijt LS, Braunstahl GJ, Leman K, Jung S, Hoogsteden HC, Lambrecht BN An essential role for dendritic cells in human and experimental allergic rhinitis. J Allergy Clin Immunol 2006 118 1117-1125. 

Li G, Hanai Y, Miyata M, et al. 1994. [Aggravating effects of chloroform and P-dichlorobenzene on experimental allergic conjunctivitis.] Folia Ophthalmol Jpn 45(5) 475-480. (Japanese)... 

Brosnan, C. F., Bronstein, M. B., and Bloom, B. R. (1981). The effects of macrophage depletion on the clinical and pathological expression of experimental allergic encephalomyelitis. J. Immunol. 126,614-620. 

Hardin-Pouzet H., Krakowski M., Bourbonniere L., Didier-Bazes M., Tran E., and Owens T. (1997). Glutamate metabolism is down-regulated in astrocytes during experimental allergic encephalomyelitis. Glia 20 79-85. 

Experimental allergic encephalomyelitis Glutamate NMDA (Hardin-Pouzet et al., 1997)... 

Paul C. and Bolton C. (2002). Modulation of blood-brain barrier dysfunction and neurological deficits during acute experimental allergic encephalomyelitis by the A-methyl-D-aspartate receptor antagonist memantine. J. Pharmacol. Exp. Ther. 302 50-57. 

Models of autoimmune diabetes in nonobese diabetic mice (NOD) mice, insulin-dependent diabetes, and experimental allergic encephalyomyelitis (EAE) were also used to evaluate naked pDNA therapy. In the latter models, a predominant Thl cytokine response is thought to play a role in disease symptoms and etiology. Treatment of these mouse models with a TH2 type cytokine, such as IL-10 or IL-4, has been found to shift the immune response and lessen the severity of disease. Therefore, the efficacy of pDNA delivery of a Th2 cytokine was explored in these specific models. 

Piccirillo, C.A. and Prud homme, G.J. (1999) Prevention of experimental allergic encephalomyelitis by intramuscular gene transfer with cytokine-encoding plasmid vectors. Hum. Gene Then, 10,1915-1922. 

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