Read e-book online Autoimmune Neurological Disease PDF


By Michael P. Pender

This publication offers a accomplished, updated and important evaluate of the immunological features of autoimmune neurological sickness. those illnesses comprise universal stipulations similar to a number of sclerosis, the Guillain-Barre syndrome, and myasthenia gravis. The e-book starts with chapters on antigen attractiveness and self-nonself acceptance, and neuroimmunology, by means of chapters on particular ailments. for every affliction, the authors hide medical beneficial properties, genetics, neuropathology, pathophysiology, immunology, and remedy. each one bankruptcy summarizes key issues and indicates instructions for destiny learn. The authors hide animal types of autoimmune neurological ailment intimately due to their value in realizing the human illnesses.

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Muscle and Nerve, 13, 106-16. F. E. (1977). Immunologically privileged sites. Advances in Immunology, 25, 1-54. C. A. (1989). Expression of MHC antigens in the central nervous system. Transplantation Proceedings, 21, 3163-5. R. & Mirsky, R. (1992). In the presence of dexamethasone, gamma interferon induces rat oligodendrocytes to express major histocompatibility complex class II molecules. Proceedings of the National Academy of Sciences USA, 89, 9054-8. W. Y. (1983). Immunohistological analysis of T lymphocyte subsets in the central nervous system in chronic progressive multiple sclerosis.

N. (1994). Nervous tissue as an immune compartment: the dialect of the immune response in the CNS. Immunology Today, 15, 218-24. , Wekerle, H. & Fontana, A. (1985). Astrocytes as antigenpresenting cells. I. Induction of la antigen expression on astrocytes by T cells via immune interferon and its effect on antigen presentation. Journal of Immunology, 134, 3785-93. , Fierz, W. & Wekerle, H. (1984). Astrocytes present myelin basic protein to encephalitogenic T-cell lines. Nature, 307, 273-6. , Schwerdel, C.

1993). When considering the relationship between the clinical and neuropathological features of EAE, it is important to know the extent of neuropathology in the PNS as well as in the 34 AUTOIMMUNE NEUROLOGICAL DISEASE CNS. For example, in rabbits with EAE induced by inoculation with whole spinal cord and CFA, demyelination-induced conduction block in the PNS, specifically the dorsal root ganglia, accounts for the ataxia and areflexia (Pender & Sears, 1982,1984,1985). In Lewis rats with MBP-EAE, conduction block due to demyelination in the spinal roots is a major cause of the neurological signs, although significant conduction block also occurs in the dorsal columns of the spinal cord (Pender, 1986a, 1988a,c; Chalk, McCombe & Pender, 1994a).

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