Immunohistochemical localisation of terminal complement component C9 in experimental allergic encephalomyelitis (original) (raw)
Summary
The deposition of terminal complement component C9 within the central nervous system (CNS) has been studied immunohistochemically in three models of experimental allergic encephalomyelitis (EAE) in the rat; inflammatory EAE induced by the passive transfer of myelin basic protein-specific T cells (tEAE), antibody-mediated, demyelinating tEAE and a subacute/chronic model induced by active immunisation with guinea pig spinal cord tissue in adjuvant. Two distinct patterns of C9 reactivity were observed, a diffuse staining of the tissue adjacent to inflammatory lesions, similar to that seen for other extra-vasculated serum proteins, and also granular, sometimes fibrillar C9 deposits around some inflammed vessels and in areas of active demyelination. The latter staining pattern was most pronounced in animals with acute antibody-mediated demyelinating tEAE, in which extensive, but transient, subpial and perivascular granular deposits of C9 were associated with regions of acute demyelination. A similar pattern of granular C9 reactivity was also associated with demyelinating lesions in animals with actively induced chronic progressive EAE. However, these C9 deposits were not observed in rats with purely inflammatory, clinically mild tEAE, although C9 deposition was occasionally observed around a small number of inflammed vessels in animals with hyperacute, lethal tEAE. These observations demonstrate that deposition of C9, the major component of the cytolytic membrane attack complex, in EAE is related to myelin injury rather than CNS inflammation.
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References
- Ben-Nun A, Wekerle H, Cohen IR (1981) The rapid isolation of clonable antigen-specific T lymphocyte lines capable of mediating autoimmune encephalomyelitis. Eur J Immunol 11:195–199
Google Scholar - Biesecker G, Muller-Eberhard HJ (1980) The ninth component of human complement: purification and physicochemical characterisation. J Immunol 124:1291–1296
Google Scholar - Campbell AK, Morgan BP (1985) Monoclonal antibodies demonstrate protection of polymorphonuclear leukocytes against complement attack. Nature 317:164–166
Google Scholar - Compston DAS, Morgan BP, Campbell AK (1987) Cercbrospinal fluid complement components in multiple sclerosis. In: Lowenthal A, Raus R (eds) Cellular and humoral immunological components of cerebrospinal fluid in multiple sclerosis. Plenum Press, New York, pp 200–209
Google Scholar - Compston DAS, Morgan BP, Campbell AK, Jasani B (1989) Immunocyto-chemical localisation of the terminal complement complex in multipe sclerosis. Neuropathol Appl Neurobiol (in press)
- De Rosbo K, Bernard CCA, Simons RD, Carnegic PR (1985) Concomitant detection of changes in myelin basic protein and permeability of blood-spinal cord barrier in acute experimental autoimmune encephalomyelitis by electroblotting. J Neuroimmunol 9:349–357
Google Scholar - Eylar EH, Jackson JJ (1974) Myelin basic proteins. Methods Enzymol 32B:323–341
Google Scholar - heininger K, Fierz W, Schafer B, Hartung H-P, Wehling P, Toyka KV (1989) Electrophysiological investigations in adoptively transferred experimental autoimmune encephalomyelitis in the Lewis rat. Brain 112:537–552
Google Scholar - Kies M (1985) Species specificity and localisation of encephalitogenic sites in myelin basic protein. Springer Semin Immunopathol 8:295–303
Google Scholar - Laemmli UK (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227:680–685
Google Scholar - Lampert PW, Carpenter S (1965) Electron microscopic studies on the vascular permeability and the mechanisms of demyelination in experimental allergic encephalomyelitis. J Neuropathol Exp Neurol 24:11–24
Google Scholar - Lassmann H (1983) Comparative neuropathology of chronic experimental allergic encephalomyelitis and multiple sclerosis, vol 25. Springer, Berlin Heidelberg New York.
Google Scholar - Lassmann H, Linington C (1988) The role of antibodies against myelin surface antigens in demyelination in chronic EAE. In: Serlupi Crescenzi G (ed) A multidisciplinary approach to myelin disease; ASI-Ser. Plenum Press, New York
Google Scholar - Lassmann H, Vass K, Brunner C, Seitelberger F (1986) Characterisation of inflammatory infiltrates in experimental allergic encephalomyelitis. Prog Neuropathol 6:33–62
Google Scholar - Lassmann H, Vass K, Brunner C, Wisniewski HM (1986) Peripheral nervous system lesions in experimental allergic encephalomyelitis: ultrastructural localisation of T cells and Ia antigen. Acta Neuropathol (Berl) 69:193–204
Google Scholar - Lassmann H, Brunner C, Bradl M, Linington C (1988) Experimental allergic encephalomyelitis: the balance between encephalitogenic T lymphocytes and demyelinating antibodies determines size and structure of demyelinated lesions. Acta Neuropathol (Berl) 75:566–576
Google Scholar - Levine S, Cochrane CG, Carpenter CB (1971) Allergic encephalomyelitis: effect of complement depletion with cobra venom. Proc Soc Exp Biol Med 138:285–289
Google Scholar - Linington C, Bradl M, Lassmann H, Brunner C, Vass K (1988) Augmentation of demyelination in rat acute allergic encephalomyelitis by circulating mouse monoclonal antibodies directed against a myelin/oligodendrocyte glycoprotein (MOG). Am J Pathol 130:443–454
Google Scholar - Linington C, Morgan BP, Scolding NJ, Piddlesden S, Wilkins P, Compston DAS (1989) The role of complement in the pathogenesis of experimental allergic encephalomyelitis. Brain (in press)
- Morariu MA, Dalmasso AP (1978) Experimental allergic encephalomyelitis in cobra venom factor-treated and C4-deficient guinea pig. Ann Neurol 4:427–430
Google Scholar - Morgan BP, Campbell AK, Compston DAS (1984) Terminal component of complement (C9) in cerebrospinal fluid of patients with multiple sclerosis. Lancet II:251–255
Google Scholar - Morgan BP, Dankert JR, Esser AF (1987) Recovery of human neutrophils from complement attack: removal of the membrane attack complex by endocytosis and exocytosis. J Immunol 138:246–253
Google Scholar - Oldstone MBA, Dixon FJ (1968) Immunohistochemical study of allergic encephalomyelitis. Am J Pathol 52:251–257
Google Scholar - Pabst H, Day NK, Gewurz H, Good RA (1971) Prevention of experimental allergic encephalomyelitis with cobra venom factor. Proc Soc Exp Biol Med 136:555–560
Google Scholar - Pender MP (1987) Demyelination and neurological signs in experimental allergic encephalomyelitis. J Neuroimmunol 15:11–24
Google Scholar - Raine CS (1986) Experimental allergic encephalomyelitis and experimental allergic neuritis. Handb Clin Neurol 47:429–466
Google Scholar - Ramm LE, Whitlow MB, Koski CL, Shin ML, Mayer MM (1983) Elimination of complement channels from the plasma membrane of U937, a nucleated mammalian cell line: temperature dependence of the elimination rate. J Immunol 131:1411–1415
Google Scholar - Sanders ME, Koski CL, Robbins D, Shin ML, Frank MM, Joiner KA (1986) Activated terminal complement in cerebrospinal fluid in Guillain-Barre syndrome and multiple sclerosis. J Immunol 136:4456–4459
Google Scholar - Schluesener H, Sobel R, Linington C, Weiner H (1987) A monoclonal antibody against a myelin/oligodendrocyte glycoprotein induces relapses and demyelination in central nervous system autoimmune disease. J Immunol 139:2505–2511
Google Scholar - Scolding NJ, Morgan BP, Houston A, Campbell AK, Linington C, Compston DAS (1989) Normal rat serum cytotoxicity against syngeneic oligodendrocytes: complement activation and attack in the absence of anti-myclin antibodies. J Neurol Sci 89:289–300
Google Scholar - Silverman BA, Carney DF, Johnston CA, Vanguri P, Shin ML (1984) Isolation of membrane attack complex of complement from myelin membranes treated with serum complement. J Neurochem 42:1024–1029
Google Scholar - Vass K, Lassmann H, Wekerle H, Wisniewski HM (1986) The distribution of Ia antigen in the lesions of rat acute experimental allergic encephalomyelitis. Acta Neuropathol (Berl) 70:149–160
Google Scholar
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Authors and Affiliations
- Section of Neurology, Department of Medicine, University of Wales, College of Medicine, Heath Park, CF4 4XN, Cardiff, Great Britain
C. Linington & D. A. S. Compston - Department of Medical Biochemistry, University of Wales, College of Medicine, Heath Park, CF4 4XN, Cardiff, Great Britain
B. P. Morgan - Neurological Institute, University of Vienna, Austria
H. Lassmann - Brain Research Institute, Austrian Academy of Sciences, CB2 2QQ, Cambridge, Great Britain
H. Lassmann - Neurology Department, Addenbrookes Hospital, CB2 2QQ, Cambridge, Great Britain
D. A. S. Compston
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Supported by the Science Research Fund (Austria), Project P6438M and the Multiple Sclerosis Society of Great Britain and Northern Ireland
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Linington, C., Lassmann, H., Morgan, B.P. et al. Immunohistochemical localisation of terminal complement component C9 in experimental allergic encephalomyelitis.Acta Neuropathol 79, 78–85 (1989). https://doi.org/10.1007/BF00308961
- Received: 29 March 1989
- Revised: 24 April 1989
- Accepted: 24 April 1989
- Issue Date: October 1989
- DOI: https://doi.org/10.1007/BF00308961