Abstract:
:Many pathological conditions of the central nervous system involve damage to and removal of myelin membrane. Very little is known about initiation of this membrane damage and the mechanisms of disposal of the damaged tissue. We are interested in the interaction between complement (the components of complement are designated C1, C2, C3, etc.) and myelin membranes and the possible role of complement in amplifying myelin damage and in the disposal of damaged myelin in vivo, because activation of complement generates both membrane-attack complexes and opsonin(s). In this study, we found that isolated rat or human myelin consumes complement in the absence of specific antibodies. Activation of complement was demonstrated by showing C3 cleavage in fresh serum incubated with myelin. Incubation of central nervous system myelin with C2-deficient serum produced no C3 consumption and only minor factor B conversion, thus excluding the alternative pathway of activation. Involvement of the classical pathway was shown directly by the C1 fixation and transfer assay. Myelin incubated with C2-deficient serum or with purified C1 and then washed contained C1 activity that could lyse sheep erythrocytes sensitized with anti-Forssman IgM antibody and carrying C4, together with C2 and C3-C9. Membranes in brain tissues other than myelin (heavy membrane fraction obtained on sucrose density gradient centrifugation) were unable to activate C1.
journal_name
Proc Natl Acad Sci U S Aauthors
Vanguri P,Koski CL,Silverman B,Shin MLdoi
10.1073/pnas.79.10.3290subject
Has Abstractpub_date
1982-05-01 00:00:00pages
3290-4issue
10eissn
0027-8424issn
1091-6490journal_volume
79pub_type
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