COMPLEMENT-FIXING ANTIBRAIN ANTIBODIES IN MULTIPLE SCLEROSIS<i>A Preliminary Report</i>

Laurell, Anna‐Brita; Link, Hans

doi:10.1111/j.1600-0404.1972.tb07567.x

Cited by 14 publications

(2 citation statements)

References 11 publications

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“…3. In selected experiments, the binding of specific immunoglobulin fractions of sera in undiluted and 1:2 dilutions was as¬ sayed, using subsequent incubation with -chain specific fluorescein-conjugated anti-IgG, anti-IgM, and anti-IgA.…”

Section: Methodsmentioning

confidence: 99%

Antimyelin Antibodies in Neurologic Diseases

1975

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Antimyelin binding activity was determined in patients with multiple sclerosis, amyotrophic lateral sclerosis, other neurologic diseases, and normals. There was an increase in the group mean titer of antimyelin antibodies in patients with multiple sclerosis (MS) in acute exacerbation, amyotrophic lateral sclerosis (ALS) and Guillain-Barré syndrome. A lesser degree of binding was found in normals of all ages. There was an increase in the incidence of antimyelin antibodies in the IgM class in patients with ALS and MS. The interaction between human immunoglobulins and myelin seems to be immunologically specific and has the nature of an antigen-antibody reaction.

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Section: Methodsmentioning

confidence: 99%

Antimyelin Antibodies in Neurologic Diseases

1975

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“…There is also increasing evidence that complement is necessary for the effector arm of this immune response (62). Complement‐fixing antibodies have been demonstrated in MS (56). In addition, late components of the complement activation system are present in the cerebrospinal fluid (CSF) of MS patients (22).…”

mentioning

confidence: 99%

Effectors of Demyelination and Remyelination in the CNS: Implications for Multiple Sclerosis

Rodriguez¹

2007

Brain Pathology

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Most of the research on multiple sclerosis (MS) has focused on the early events that trigger demyelination and subsequent remyelination. Less attention has been given to the factors that directly mediate the demyelination that is the hallmark of the disease. Effector cells or molecules are those factors directly responsible for mediating the damage in the disease. Similarly, there are effector molecules that are critical for remyelination in the central nervous system (CNS). By understanding those effector molecules in demyelination and remyelination that directly influence the pathologic process, we should be able to generate specific therapies with the greatest potential for benefiting MS patients. This review focuses on effector cells and molecules that are critical for demyelination and remyelination in MS but also in experimental models of the disease including experimental autoimmune encephalomyelitis (EAE), virus-induced models of demyelination (Theiler's virus, murine hepatitis virus), and toxic models of demyelination (lysolecithin, ethidium bromide, and cuprizone). These are models in which the effector molecules for demyelination and remyelination have been most precisely evaluated.

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Autoantibodies to Neural and Non-neural Antigens in Multiple Sclerosis

Ryberg¹

1987

Cellular and Humoral Immunological Components of Cerebrospinal Fluid in Multiple Sclerosis

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COMPLEMENT-FIXING ANTIBRAIN ANTIBODIES IN MULTIPLE SCLEROSISA Preliminary Report

Cited by 14 publications

References 11 publications

Antimyelin Antibodies in Neurologic Diseases

Antimyelin Antibodies in Neurologic Diseases

Effectors of Demyelination and Remyelination in the CNS: Implications for Multiple Sclerosis

Autoantibodies to Neural and Non-neural Antigens in Multiple Sclerosis

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