Neuropathology in multiple sclerosis: new concepts

Multiple sclerosis lesions are characterized by inflammation, demyelination and a variable degree of axonal loss. The patterns of inflammation in MS lesions are compatible with a T-lymphocyte mediated immune reaction. The formation of demyelinated plaques, however, seem to require additional immunological mechanisms. In this review evidence is discussed for a pathogenetic role of demyelinating antibodies, toxic macrophage products, cytotoxic T-cells as well as metabolic disturbances of oligodendrocytes. It is suggested that the pathological heterogeneity regarding the patterns and extent of demyelination, remyelination and axonal loss may be the outcome of variable dominant immunopathogenetic mechanisms in different multiple sclerosis patients.

[1]  C. Godfraind,et al.  Expression of viral and myelin gene transcripts in a murine CNS demyelinating disease caused by a coronavirus , 2004, Glia.

[2]  H. Lassmann,et al.  Multiple sclerosis: In situ evidence for antibody‐ and complement‐mediated demyelination , 1998, Annals of neurology.

[3]  H. Lassmann,et al.  Experimental autoimmune encephalomyelitis: the antigen specificity of T lymphocytes determines the topography of lesions in the central and peripheral nervous system. , 1997, Laboratory investigation; a journal of technical methods and pathology.

[4]  H. Lassmann,et al.  Dying‐back oligodendrogliopathy: A late sequel of myelin‐associated glycoprotein deficiency , 1997, Glia.

[5]  H. Lassmann,et al.  Patterns of oligodendrocyte pathology in coronavirus‐induced subacute demyelinating encephalomyelitis in the lewis rat , 1997, Glia.

[6]  S. Hauser,et al.  Late Complications of Immune Deviation Therapy in a Nonhuman Primate , 1996, Science.

[7]  J. Antel,et al.  Multiple Sclerosis: Fas Signaling in Oligodendrocyte Cell Death , 1996, The Journal of experimental medicine.

[8]  J. Menonna,et al.  Involvement of the CD95 (APO-1/Fas) receptor/ligand system in multiple sclerosis brain , 1996, The Journal of experimental medicine.

[9]  A. Taniguchi,et al.  Role of SOD-1 and nitric oxide/cyclic GMP cascade on neurofilament aggregation in ALS/MND , 1996, Journal of the Neurological Sciences.

[10]  D. Hinds,et al.  A full genome search in multiple sclerosis , 1996, Nature Genetics.

[11]  J. Haines,et al.  A complete genomic screen for multiple sclerosis underscores a role for the major histocompatability complex , 1996, Nature Genetics.

[12]  P. Goodfellow,et al.  A genome screen in multiple sclerosis reveals susceptibility loci on chromosome 6p21 and 17q22 , 1996, Nature Genetics.

[13]  Moses Rodriguez,et al.  Central Nervous System Remyelination Clinical Application of Basic Neuroscience Principles , 1996, Brain pathology.

[14]  Moses Rodriguez,et al.  Distinct Patterns of Multiple Sclerosis Pathology Indicates Heterogeneity in Pathogenesis , 1996, Brain pathology.

[15]  A. Thompson,et al.  Spinal cord atrophy and disability in multiple sclerosis. A new reproducible and sensitive MRI method with potential to monitor disease progression. , 1996, Brain : a journal of neurology.

[16]  W. Blakemore,et al.  Failure to achieve remyelination of demyelinated rat axons following transplantation of glial cells obtained from the adult human brain , 1996, Neuropathology and applied neurobiology.

[17]  H. Lassmann,et al.  The N-terminal domain of the myelin oligodendrocyte glycoprotein (MOG) induces acute demyelinating experimental autoimmune encephalomyelitis in the Lewis rat , 1995, Journal of Neuroimmunology.

[18]  G. Kollias,et al.  Spontaneous inflammatory demyelinating disease in transgenic mice showing central nervous system-specific expression of tumor necrosis factor alpha. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[19]  Hans Lassmann,et al.  Monocyte/macrophage differentiation in early multiple sclerosis lesions , 1995, Annals of neurology.

[20]  C. Goodyer,et al.  Differential susceptibility of human CNS-derived cell populations to TNF-dependent and independent immune-mediated injury , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[21]  P. A. Schad,et al.  Plaque-associated expression of human herpesvirus 6 in multiple sclerosis. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[22]  C. Polman,et al.  The small heat-shock protein αB-crystallin as candidate autoantigen in multiple sclerosis , 1995, Nature.

[23]  T. Johns,et al.  Myelin oligodendrocyte glycoprotein induces a demyelinating encephalomyelitis resembling multiple sclerosis. , 1995, Journal of immunology.

[24]  H. Weiner,et al.  Immunologic Mechanisms and Therapy in Multiple Sclerosis , 1995, Immunological reviews.

[25]  C. Raine,et al.  The adhesion molecule and cytokine profile of multiple sclerosis lesions , 1995, Annals of neurology.

[26]  K. Jellinger,et al.  Patterns of oligodendroglia pathology in multiple sclerosis. , 1994, Brain : a journal of neurology.

[27]  O. Majdic,et al.  Identification of epitopes of myelin oligodendrocyte glycoprotein for the induction of experimental allergic encephalomyelitis in SJL and Biozzi AB/H mice. , 1994, Journal of immunology.

[28]  K. Mikoshiba,et al.  Glial cell degeneration and hypomyelination caused by overexpression of myelin proteolipid protein gene , 1994, Neuron.

[29]  H. Lipp,et al.  Mice deficient for the glycoprotein show subtle abnormalities in myelin , 1994, Neuron.

[30]  J. Newcombe,et al.  Low density lipoprotein uptake by macrophages in multiple sclerosis plaques: implications for pathogenesis , 1994, Neuropathology and applied neurobiology.

[31]  C. Readhead,et al.  Premature arrest of myelin formation in transgenic mice with increased proteolipid protein gene dosage , 1994, Neuron.

[32]  Moses Rodriguez,et al.  Proteolipid Protein Gene Expression in Demyelination and Remyelination of the Central Nervous System: A Model for Multiple Sclerosis , 1994, Journal of neuropathology and experimental neurology.

[33]  J. Antel,et al.  Reactive microglia in multiple sclerosis lesions have an increased expression of receptors for the Fc part of IgG , 1994, Journal of the Neurological Sciences.

[34]  P. Dore‐Duffy,et al.  Expression of immunologically relevant endothelial cell activation antigens on isolated central neurvous system microvessels from patients with multiple sclerosis , 1994, Annals of neurology.

[35]  W. Brück,et al.  Oligodendrocytes in the early course of multiple sclerosis , 1994, Annals of neurology.

[36]  M. Cuzner,et al.  Cytokine mRNA expression in inflammatory multiple sclerosis lesions: detection by non-radioactive in situ hybridization. , 1993, Cytokine.

[37]  P. Kelly,et al.  Oligodendrocyte injury is an early event in lesions of multiple sclerosis. , 1993, Mayo Clinic proceedings.

[38]  T Revesz,et al.  Multiple sclerosis. Pathology of recurrent lesions. , 1993, Brain : a journal of neurology.

[39]  E. Cho,et al.  Multiple sclerosis: Remyelination of nascent lesions: Remyelination of nascent lesions , 1993 .

[40]  B. Engelhardt,et al.  Induction of persistently demyelinated lesions in the rat following the repeated adoptive transfer of encephalitogenic T cells and demyelinating antibody , 1992, Journal of Neuroimmunology.

[41]  D. Hafler,et al.  T cell receptor V alpha-V beta repertoire and cytokine gene expression in active multiple sclerosis lesions , 1992, The Journal of experimental medicine.

[42]  C. Brosnan,et al.  Cytokine cytotoxicity against oligodendrocytes. Apoptosis induced by lymphotoxin. , 1991, Journal of immunology.

[43]  C. Brosnan,et al.  Colocalization of lymphocytes bearing gamma delta T-cell receptor and heat shock protein hsp65+ oligodendrocytes in multiple sclerosis. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[44]  C. Brosnan,et al.  Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions. , 1991, The Journal of clinical investigation.

[45]  M. Esiri,et al.  Blood-brain barrier damage in acute multiple sclerosis plaques. An immunocytological study. , 1991, Brain : a journal of neurology.

[46]  B. Morgan,et al.  Oligodendrocyte susceptibility to injury by T-cell perforin. , 1990, Immunology.

[47]  J. Merrill,et al.  Tumor necrosis factor identified in multiple sclerosis brain , 1989, The Journal of experimental medicine.

[48]  A. Campbell,et al.  Normal rat serum cytotoxicity against syngeneic oligodendrocytes Complement activation and attack in the absence of anti-myelin antibodies , 1989, Journal of the Neurological Sciences.

[49]  K. Selmaj,et al.  Tumor necrosis factor mediates myelin and oligodendrocyte damage in vitro , 1988, Annals of neurology.

[50]  H. Lassmann,et al.  Augmentation of demyelination in rat acute allergic encephalomyelitis by circulating mouse monoclonal antibodies directed against a myelin/oligodendrocyte glycoprotein. , 1988, The American journal of pathology.

[51]  R. Fujinami,et al.  Mechanism of Theiler's virus-induced demyelination in nude mice. , 1986, Laboratory investigation; a journal of technical methods and pathology.

[52]  N. J. Pressman,et al.  A quantitation of myelin‐associated glycoprotein and myelin basic protein loss in different demyelinating disease , 1985, Annals of neurology.

[53]  E. Cho,et al.  Continual Breakdown and Regeneration of Myelin in Progressive Multiple Sclerosis Plaques a , 1984, Annals of the New York Academy of Sciences.

[54]  E. Reinherz,et al.  Multiple sclerosis Distribution of T cells, T cell subsets and Ia-positive macrophages in lesions of different ages , 1983, Journal of Neuroimmunology.

[55]  L. Scheinberg,et al.  Multiple sclerosis. Oligodendrocyte survival and proliferation in an active established lesion. , 1981, Laboratory investigation; a journal of technical methods and pathology.

[56]  J. Prineas,et al.  Multiple sclerosis: Capping of surface immunoglobulin G on macrophages engaged in myelin breakdown , 1981, Annals of neurology.

[57]  I. Grundke‐Iqbal,et al.  Multiple sclerosis , 1980, Neurology.

[58]  M. Esiri IMMUNOGLOBULIN-CONTAINING CELLS IN MULTIPLE-SCLEROSIS PLAQUES , 1977, The Lancet.

[59]  S. Appel,et al.  TISSUE CULTURE STUDIES OF DEMYELINATION * , 1965, Annals of the New York Academy of Sciences.

[60]  A. Blalock Surgical treatment of pulmonary stenosis. , 1947, Lancet.

[61]  J. Baló ENCEPHALITIS PERIAXIALIS CONCENTRICA , 1928 .

[62]  P. Schilder Zur Kenntnis der sogenannten diffusen Sklerose. (Über Encephalitis periaxialis diffusa.) , 1912 .

[63]  H. Lassmann,et al.  Histopathology and the blood–cerebrospinal fluid barrier in multiple sclerosis , 1994, Annals of neurology.

[64]  D. Kirschner,et al.  Mice deficient for the myelin-associated glycoprotein show subtle abnormalities in myelin. , 1994, Neuron.

[65]  E. Cho,et al.  Multiple sclerosis: remyelination of nascent lesions. , 1993, Annals of neurology.

[66]  S. Markey,et al.  Human macrophages convert L-tryptophan into the neurotoxin quinolinic acid. , 1992, The Biochemical journal.

[67]  M. Freedman,et al.  Peripheral blood gamma-delta T cells lyse fresh human brain-derived oligodendrocytes. , 1991, Annals of neurology.

[68]  R. Stocker,et al.  Selective degeneration of oligodendrocytes mediated by reactive oxygen species. , 1990, Free radical research communications.

[69]  J. Olney Excitotoxins: An Overview , 1983 .

[70]  Dr. med. Hans Lassmann Comparative Neuropathology of Chronic Experimental Allergic Encephalomyelitis and Multiple Sclerosis , 1983, Schriftenreihe Neurologie / Neurology Series.

[71]  I. Cohen,et al.  The rapid isolation of clonable antigen‐specific T lymphocyte lines capable of mediating autoimmune encephalomyelitis , 1981, European journal of immunology.

[72]  C. Brosnan,et al.  Colocalization of lymphocytes bearing v6 T-cell receptor and heat shock protein hsp65' oligodendrocytes in multiple sclerosis , 2022 .