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Immunohistochemical localisation of terminal complement component C9 in experimental allergic encephalomyelitis
C Linington1, H Lassmann, B P Morgan
1Department of Medicine, University of Wales, College of Medicine, Heath Park, Cardiff, Great Britain.
Acta Neuropathologica
|January 1, 1989
Summary
Terminal complement component C9 deposition in the central nervous system (CNS) is linked to myelin injury, not inflammation, in experimental allergic encephalomyelitis (EAE) models. This finding highlights C9
Area of Science:
- Neuroimmunology
- Immunopathology
- Complement System
Background:
- Experimental allergic encephalomyelitis (EAE) is a model for CNS inflammatory demyelinating diseases.
- The terminal complement component C9 is a key component of the membrane attack complex (MAC).
Purpose of the Study:
- To investigate the deposition patterns of C9 in the CNS during different models of EAE.
- To determine the relationship between C9 deposition and CNS inflammation versus myelin injury in EAE.
Main Methods:
- Immunohistochemical analysis of C9 deposition in rat models of EAE.
- Comparison of C9 staining patterns in inflammatory, demyelinating, and chronic EAE models.
Main Results:
- Two distinct C9 deposition patterns were observed: diffuse and granular.
- Granular C9 deposits were associated with areas of active demyelination, particularly in antibody-mediated and chronic EAE.
- C9 deposition correlated with myelin injury, not solely with CNS inflammation or inflammatory cell infiltration.
Conclusions:
- Terminal complement component C9 deposition in EAE is primarily associated with myelin damage.
- The localization of C9 suggests a role in demyelination rather than being a general marker of CNS inflammation.