Role of complement in demyelination in vitro by multiple sclerosis serum and other neurological disease sera

Bradbury, K.; Aparicio, S. R.; Sumner, David; Bird, C. C.

doi:10.1016/0022-510x(84)90092-3

Cited by 19 publications

(8 citation statements)

References 20 publications

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“…This can explain the therapeutic efficacy of immunoadsorption. The repeated removal of complement components [16,18] and total serum immunoglobulins decreases the number of disease‐associated antibodies, thereby reducing local and systemic pathogenic factors involved in demyelination [22,23]. As expected, our laboratory analyses demonstrated a reduction of IgG and IgM to one‐third of baseline values coinciding with a decrease in anti‐MOG antibodies in the patients’ sera and high anti‐MOG concentrations in the column eluates.…”

Section: Discussionsupporting

confidence: 70%

“…This can explain the therapeutic efficacy of immunoadsorption. The repeated removal of complement components [16,18] and total serum immunoglobulins decreases the number of disease-associated antibodies, thereby reducing local and systemic pathogenic factors involved in demyelination [22,23]. As expected, our laboratory Each patient's EDSS scores, represented by round circles (a), and median change of the EDSS score (b) from 6 months prior to baseline until the last immunoadsorption (3 months) and at 6 and 12 months follow-up.…”

Section: Discussionsupporting

confidence: 65%

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Immunoadsorption patients with multiple sclerosis: an open‐label pilot study

Moldenhauer

Haas

Wäscher

et al. 2005

Eur J Clin Investigation

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Section: Discussionsupporting

confidence: 70%

“…This can explain the therapeutic efficacy of immunoadsorption. The repeated removal of complement components [16,18] and total serum immunoglobulins decreases the number of disease-associated antibodies, thereby reducing local and systemic pathogenic factors involved in demyelination [22,23]. As expected, our laboratory Each patient's EDSS scores, represented by round circles (a), and median change of the EDSS score (b) from 6 months prior to baseline until the last immunoadsorption (3 months) and at 6 and 12 months follow-up.…”

Section: Discussionsupporting

confidence: 65%

Immunoadsorption patients with multiple sclerosis: an open‐label pilot study

Moldenhauer

Haas

Wäscher

et al. 2005

Eur J Clin Investigation

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“…These two proteins are functionally identical to Cl and cleave C4 and C2, leading to the formation of a classical pathway C3-convertase. Of particular interest is the fact that myelin and myelin basic protein can activate both the classical and alternative pathways, in the presence or absence of myelin-specific antibodies, and activation results in the hydrolysis of myelin and myelin basic protein (Cyong et al, 1982;Vanguri et al, 1982;Bradbury et al, 1984;Silberberg et al, 1984;Vanguri and Shin, 1988;Linington et al, 1989). Thus, regardless of the etiologic events that cause myelin damage and breakdown, myelin-induced activation of complement can likely enhance inflammation and tissue destruction mediated by complement.…”

Section: The Complement Systemmentioning

confidence: 99%

Complement Biosynthesis in the Central Nervous System

Barnum

1995

Critical Reviews in Oral Biology & Medicine

187

103

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ABSTRACT:Complement is an important effector arm of the human immune response. Binding of proteolytic fragments derived from activation of complement by specific receptors leads to responses as diverse as inflammation, opsonization, and B-cell activation. The importance of characterizing the expression and regulation of complement in the CNS is highlighted by growing evidence that complement plays a significant role in the pathogenesis of a variety of neurological diseases, such as multiple sclerosis and Alzheimer's disease. \n vitro studies have demonstrated that astrocytes, the predominant glial cell type in the brain, are capable of expressing or producing a majority of the components of the complement system. Expression of many complement proteins synthesized by astrocytes is regulated by both pro-and anti-inflammatory cytokines, many of which are also produced by several cell types in the CNS. In addition to astrocytes, ependymal cells, endothelial cells, microglia, and neurons have recently been shown to synthesize various complement proteins or express complement receptors on their cell surfaces. Together, these studies demonstrate that several cell types throughout the brain have the potential to express complement and, in many cases, increase expression in response to mediators of the acute phase response. These studies suggest that complement may play a greater role in CNS immune responses than previously thought, and pave the way for better understanding of the dynamics of complement expression and regulation in vivo. Such understanding may lead to therapeutic manipulation of complement host defense functions in a variety of inflammatory and degenerative diseases in the CNS.

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“…Andererseits scheinen (Auto-)Antikörper bzw. Immunkomplexe gegen Bestandteile der Nervenscheide das Komplementsystem zu aktivieren (17,18), u. a. auch den alternativen Weg im Blut bei Multipler Sklerose (19). Jedenfalls konnte mittels einer Myelinfraktion aus peripherem Nerv der alternative Weg des Komplementsystems aktiviert werden (20).…”

Section: Anleitungunclassified