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Immunocytochemical localization of the terminal complement complex in multiple sclerosis
D A Compston1, B P Morgan, A K Campbell
1Department of Neurology, University of Wales College of Medicine, Heath Park, Cardiff.
Insights
Complement system activation, indicated by C9 deposits, is observed in multiple sclerosis (MS) brain tissue. This suggests a role for complement in the immune-mediated tissue damage characteristic of MS.
Area of Science:
- Neurology
- Immunology
- Pathology
Background:
- Multiple sclerosis (MS) is a chronic inflammatory disease affecting the central nervous system.
- The pathogenesis of MS involves complex interactions between immune cells, inflammatory mediators, and the blood-brain barrier.
- The role of the complement system in MS pathogenesis remains an area of active investigation.
Purpose of the Study:
- To investigate the presence and localization of complement system components in MS brain tissue.
- To determine if complement activation is associated with focal tissue damage in MS plaques.
Main Methods:
- Immunocytochemical analysis of post-mortem brain tissue from MS patients and controls.
- Detection of C9 and the terminal complement complex.
- Association of deposits with capillary endothelial cells within plaques and white matter.
Main Results:
- Granular deposits of C9 and the terminal complement complex (0.3-1.2 microns) were found in 5/7 MS patients and one patient with subacute sclerosing panencephalitis.
- These deposits were associated with capillary endothelial cells, predominantly in plaques and adjacent white matter.
- No such deposits were observed in control individuals (7/7).
Conclusions:
- The findings suggest that complement activation occurs in the context of MS.
- Complement activation may be involved in the focal tissue damage observed in MS.
- This process may involve the passage of immune mediators across the blood-brain barrier.
Abstract:
Granular deposits of C9 and the terminal complement complex, measuring 0.3-1.2 microns, have been demonstrated immunocytochemically in association with capillary endothelial cells, predominantly within plaques and adjacent white matter, in tissue obtained at autopsy from 5/7 patients with multiple sclerosis (MS) and one individual with subacute sclerosing panencephalitis but not from 7/7 controls. This finding suggests that the evolution of focal tissue damage in MS may involve complement activation associated with passage of humoral and cellular mediators of the immune system through the blood-brain barrier.
