Summary
In recent years, considerable interest has focused on the possibility that in experimental allergic encephalomyelitis (EAE), antigens other than myelin basic protein (MBP) may be required for the initiation of demyelination and for the development of exacerbating-remitting disease. Previous results from these laboratories have implicated a role for antibodies against galactocerebroside (GC) in initiating demyelination of central nervous system (CNS) tissue in vitro (8) and in vivo (9). We have now used the rabbit eye model to dissect further the role of antibodies in causing CNS demyelination. The results show: that in animals directly sensitized against GC, no spontaneous CNS lesion develops but primary demyelination is observed if a mononuclear inflammatory reaction is superimposed; that in rabbits sensitized against MBP, antiserum against GC causes enhanced demyelination; and that in normal animals, anti-GC serum initiates primary demyelination only when an inflammatory reaction is induced by supernatants of activated lymphocytes. Injection of anti-GC serum alone has no pathologic effect. These results suggest that antibodies against lipid haptens are capable of causing primary demyelination in the CNS in vivo but that effector cells provided by an inflammatory response are required. Thus, the development of the fully demyelinating lesion probably depends on both cellular and humoral mechanisms.
Keywords
- Myelin Basic Protein
- Experimental Allergic Encephalomyelitis
- Organotypic Culture
- Passive Transfer
- Central Nervous System Demyelination
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References
Raine CS, Scheinberg L, and JM Waltz (1981) Multiple Sclerosis: Oligodendrocyte survival and proliferation in an active established lesion. Lab. Invest. 45: 534–546.
Traugott U and CS Raine (1982) T and B cell distribution in Multiple sclerosis lesions. J. Neuropath Exptl. Neurol. 414: 382.
Kies MW (1965) Chemical studies on an encephalitogenic protein from guinea pig brain. Ann N.Y. Acad. Sci. 122: 161–169.
Paterson PY (1976) In Textbook of Immunopathology, (eds Meischer PA and Muller-Iberhard HJ) 179–213 ( Grune and Stratton, New York ).
Ortiz-Ortiz L and WO Weigle (1976) Cellular events in the induction of allergic encephalomyelitis in rats. J.Exp.Med. 144: 604–616
Bornstein MB and SH Appel (1961) The application of tissue culture to the study of experimental allergic encephalomyelitis. Patterns of demyelination. J.Neuropath,. Exptl. Neurol. 20: 141–157.
Bornstein MB (1978) Immunobiology of demyelination. In: Waksman SG (ed) Physiology and Pathology of Axons, Raven Press, New Yok, 313–336.
Raine CS and MB Bornstein (1976) The initial structural lesion in serum-induced demyelination in vitro. Lab. Invest. 35: 391–401.
Raine CS, Johnson AB, Marcus DM, Suzuki A and MB Bornstein, (1981) Demyelination in vitro: Absorption studies demonstrate that galactocerebroside is a major target. J.Neurol. Sci. 52: 117–131.
Seil FJ, Falk GA, Kies MW and EC Alford (1968) In vitro demyelinating activity of serum of guinea pigs sensitized with whole CNS tissue and with purified encephalitogen. Exptl. Neurol. 22: 545.
Dubois-Dalcq M, Niedieck B and M Buyse (1970) Action of anti-cerebroside sera on myelinated nervous tissue cultures. Pathologica Europa. 5: 331–347.
Fry JM, Weissbarth S, Lehrer GM and MB Bornstein (1974) Cerebroside antibody inhibits sulfatide synthesis and demyelinates in cord tissue cultures. Science 183: 540–542.
Lebar R, Boutry JM, Vincent C, Robinaux R, and GA Voisin (1976) Studies on autoimmune encephalomyelitis in the guinea pig. II. An in vitro investigation of the nature, properties and specificity of the serum demyelinating factor. J. Immunol. 116: 1439–1446.
Raine CS, Traugott U, Farooq M, Bornstein MB and WT Norton (1981) Augmentation of immune-mediated demyelination by lipid haptens. Lab Invest. 45: 174–182.
Brosnan CF, Stoner GL, Bloom BR and HM Wisniewski (1977) Studies on demyelination by activated lymphocytes in the rabbit eye. II. Antibody-dependent cell-mediated demyelination. J.Immunol. 118: 2103.
Oldstone MBA and FJ Dixon (1968) Immunohistochemical study of allergic encephalomyelitis. Amer J. Path 52: 251–257.
Grundke-Iqbal I, Lassmann H and HM Wisniewski (1980) Immunohistochemical studies in chronic relapsing experimental allergic encephalomyelitis. Arch. Neurol. 374: 651–656.
Traugott U, Shevach E, Chiba J, Stone SH, and CS Raine (1982) Chronic relapsing allergic encephalomyelitis: Identification and dynamics of T and B cells within the central nervous system. Cell. Immunol 68: 261–275.
Saida T, Saida K, Dorfman S, Brown MJ, Lisak RP, Manning M and DH Silberberg (1979) Experimental allergic neuritis (EAN) induced by sensitization with galactocerebroside. Science 204: 1103.
Saida T, Saida K, Silberberg DH, and MJ Brown (1978) Transfer of demyelination by intraneural injection of experimental allergic neuritis serum. Nature 272: 639–641.
Wisniewski HM and BR Bloom (1975) Primary demyelination as a non-specific consequence of a cell-mediated reaction. J.Exp.Med. 141: 346
Lebar R, Vincent C and E Fisher-Le Boubennec (1979) Studies on autoimmune encephalomyelitis in the guinea pig. III. A comparative study of two autoantigens of central nervous system myelin. J. Neurochem. 32: 1451–1460.
Folch J and M Lees (1951) Proteolipidsf a new type of tissue lipoprotein, their isolation from brain. J. Biochem. 191: 807–820.
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© 1983 Springer-Verlag
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Brosnan, C.F., Traugott, U., Raine, C.S. (1983). Analysis of Humoral and Cellular Events and the Role of Lipid Haptens During CNS Demyelination. In: Waksman, B.H., Yonezawa, T., Lassmann, H. (eds) Inflammation and Demyelination in the Central Nervous System. Acta Neuropathologica Supplementum, vol 9. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-69094-5_7
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DOI: https://doi.org/10.1007/978-3-642-69094-5_7
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