Advances in the Immunopathogenesis of Multiple Sclerosis by P. A. Muraro, A. Lugaresi, D. Gambi (auth.), D. Gambi, P. A.

By P. A. Muraro, A. Lugaresi, D. Gambi (auth.), D. Gambi, P. A. Muraro, A. Lugaresi, U. Ecari (eds.)

P.A. MURARO, A. LUGARESI, D. GAMBI the various pathological features of a number of sclerosis (MS) lesions were recognized for over a century. it's only lately, even though, that diversified styles of demyelination were associated with specific pathways of immune-mediated tissue destruction. specifically, the inter-individual heterogeneity of MS lesions has instructed that varied mechanisms may possibly act in numerous sufferers, accounting for the range saw in scientific path, immunological findings in peripheral blood and cere­ brospinal fluid (CSF), and reaction to immunomodulatory remedies. to supply an outline of the fundamental mechanisms potentially all in favour of MS lesion initiation and improvement, a global assembly used to be equipped within the context of the once a year Congress of the Italian Neuroimmunology organization (AINI), held on the collage of Chieti, in Chieti Italy on 29 October 1998. The excessive typical of shows caused us to file them in prolonged shape, to focus on fresh seasoned­ gress within the knowing of simple mechanisms maintaining MS immuno­ pathogenesis. A valuable function within the attainable mechanisms resulting in myelin destruc­ tion has been attributed to T lymphocytes reactive to myelin antigens. reviews at the myelin antigen-specific T mobilephone repertoire have contributed major advances to our wisdom of autoimmunity (Chapters 1,2).

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NGF and NT-3, but not BDNF, directly acted on microglia cells isolated in culture and inhibited MHC class II expression via the p7S neurotrophin receptor [13]. BDNF probably was having an indirect effect on microglial MHC class II expression in tissue culture. This effect might have been mediated by neurons releasing NGF in response to stimulation by BDNF. Neurons not only controlled MHC expression of neighboring glial cells, but also their own expression of MHC class I molecules [15]. MHC Neuronal control of the immunological microenvironment in the CNS 41 class I gene transcripts were analyzed in dissociated hippocampal neurons by combining patch-clamp electrophysiology and single cell reverse transcriptase polymerase chain reaction (RT-PCR).

Thus, immune cells and the immunological milieu can be both harmful and helpful to neurons. However, in most cases the direct contribution of the immune milieu to neuronal survival is still to be elucidated. Summary Microenvironmental factors have a profound influence on resident cell populations and their ability to modulate an immune response. The unique central nervous system (CNS) microenvironment has important effects in this regard, resulting in the establishment of immune privilege. In the CNS, neurons control the expression of "immunologically-relevant" molecules such as the major histocompatibility complex (MHC) and proinflammatory cytokines.

Neumann H, Cavalie A, Jenne DE, Wekerle H (1995) Induction of MHC class I genes in neurons. Science 269:549-552 16. Neumann H, Schmidt H, Cavalie A, Jenne D, Wekerle H (1997) MHC class I gene expression in single neurons of the central nervous system: Differential regulation by interferon-y and tumor necrosis factor-a. J Exp Med 185:305-316 17. Corriveau RA, Huh GS, Shatz CJ (1998) Regulation of class I MHC gene expression in the developing and mature CNS by neural activity. Neuron 21:505-520 18.

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