Cell-mediated immunity in idiopathic polyneuritis

Iqbal, Aleem; Oger, Joél; Arnason, Barry G. W.

doi:10.1002/ana.410090711

Cited by 71 publications

(17 citation statements)

References 34 publications

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“…(24)(25)(26), but none of these has been shown to be immunologically involved in humans (27). It is unlikely that the paraproteins share antigenic specificity with anticerebroside antibodies because there was no immunostaining of neuropathy-associated proteins by anticerebroside antiserum and because the paraproteins did not react with rabbit PNM or with chloroform/methanol-treated human PNM (9, 10) which contain cerebrosides.…”

Section: Discussionmentioning

confidence: 99%

Plasma cell dyscrasia and peripheral neuropathy: identification of the myelin antigens that react with human paraproteins.

Latov¹,

Braun²,

Gross³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

136

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In some cases of polyneuropathy and plasma cell dyscrasia, the monclonal antibodies react with human peripheral nerve myelin. To identify the myelin antigens involved, we separated the proteins of human central and peripheral nerve myelin by polyacrylamide gel electrophoresis, transferred the proteins onto nitrocellulose sheets, and used an immunoenzymatic technique to detect the reactive antigens. Serum IgM but not IgG from three patients with neuropathy and complement-fixing anti-human myelin IgM paraproteins immunostained a protein of approximately 100,000 daltons in human peripheral nerve myelin and a protein or closely migrating proteins of similar size in human central nervous system myelin. In a fourth patient, both IgM and IgG immunostained the antigen. Immunostaining was specific for the paraprotein light chain type, and absorption of the patients' sera with human peripheral nerve myelin eliminated the reaction with the central nervous system proteins. No reaction was seen with rabbit peripheral nerve myelin or with membranes prepared from human myotubes, human T cells, or human fibroblasts. Control sera from six patients with neuropathy and IgM paraproteins that did not react with myelin, from four patients with IgM paraproteins but no neuropathy, and from three normal subjects did not immunostain myelin.

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Section: Discussionmentioning

confidence: 99%

Plasma cell dyscrasia and peripheral neuropathy: identification of the myelin antigens that react with human paraproteins.

Latov¹,

Braun²,

Gross³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

136

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“…A variety of immunological abnormalities have been reported in GBS. Cell-mediated immunity to P2 protein has been reported in GBS [1,79] but not confirmed by others [40,94]. Reports that GBS peripheral blood lymphocytes can demyelinate myelinated cultures in vitro [3] cannot be taken as evidence of the cytotoxic capability of these cells due to the differences in the major histocompatibility complex of effector cells and target tissues.…”

Section: Association Of C Jejuni Infection and Gbs Was First Reportementioning

confidence: 95%

Guillain-Barr� syndrome: clinical and immunological aspects

Rostami¹

1995

Springer Semin Immunopathol

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Immune-mediated PNS disorders comprise a significant segment of diseases of the nervous system. Studies on GBS as a prototype of these disorders and its experimental model EAN have helped to elucidate some of the mechanisms responsible for myelin injury in the PNS. These mechanisms, although partially understood have been useful in implementing therapies such as plasmapheresis and IVIG and various other immunomodulators. The question of whether an infectious agent such as a virus can directly damage the myelin sheath and/or Schwann cells or whether the agent triggers an immune response against self through antigenic mimicry remains unanswered. The association between C. jejuni infection and GBS has opened new areas of investigation in understanding the immunopathogenesis of the disease. Similar observations with other environmental factors may be made in the future, pointing to the possibility that GBS may not be caused by a single agent but could be the result of an immunological attack on the PNS myelin assembly by a variety of agents or factors. Regardless of the etiology, if the myelin injury is aggravated by product of the immune cells, such as various cytokines, neutralization of these factors could help lessen the burden of injury to the nerves. Future research in autoimmune disorders of the PNS needs to focus on identifying environmental factors that directly, or indirectly through antigen mimicry, damage the PNS myelin. In parallel, further understanding of the immunopathogenesis by dissecting the immunological phenomenon at the systemic and local levels, especially the role of cytokines, growth factors, and adhesion molecules will pave the way for more rational therapies, even if the causative factors are not known. Studies in laboratory animals have demonstrated the efficacy of selective immunotherapy through modulation of the trimolecular complex, i.e., T cell receptor, MHC/molecule, and antigen. Immunological tolerance, presumably through deletion of autoreactive clones, clonal anergy, or active suppression, has proven effective in animals. Other modes of immunotherapy such as nonspecific depletion of T or B cells or down-regulation of activated cells have also been shown to abolish or decrease the severity of experimental autoimmune neurological disorders, including EAN. These immunotherapeutic modalities may become applicable to human autoimmune neuropathies.

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“…Both humoral [l] and cellular [2) immune mechanisms are thought to be involved. In GBS, transient neurological symptoms are associated with an inflammatory demyelination of peripheral nerve in which myelin is the target of the immune attack [3,41.…”

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confidence: 99%

Antibody detection in Guillain-Brr� syndrome

Svennerholm

Fredman

1990

Ann Neurol.

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Chromatograms with appropriate separated ganglioside fractions were overlaid with diluted patient sera, and antibody binding was detected with an alkaline phosphatase-labelled second antibody. Antiganglioside antibodies were present in the sera of 39 of 50 patients with Guillain-Barré syndrome (GBS), in 10 of 12 patients with Alzheimer's disease, and in approximately 30% of the controls. The antibodies were directed against ganglioside 3'-LM1, shown to be the major ganglioside of peripheral nerve (femoral nerve and cauda equina) in most of the positive GBS sera but also in a high proportion in the controls. No correlation was found between the severity or the course of the disease and the antibody titer. Daily parenteral administration of purified bovine brain-derived GM1 ganglioside for three months to 12 patients with Alzheimer's disease did not result in any antiganglioside GM1 antibodies. We have interpreted our findings in the following way. Human sera normally contain naturally occurring antibodies against gangliosides that in general do not cause any tissue damage. Thus, parenteral injection of gangliosides will not lead to any antibody formation.

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Cell-mediated immunity in idiopathic polyneuritis

Cited by 71 publications

References 34 publications

Plasma cell dyscrasia and peripheral neuropathy: identification of the myelin antigens that react with human paraproteins.

Plasma cell dyscrasia and peripheral neuropathy: identification of the myelin antigens that react with human paraproteins.

Guillain-Barr� syndrome: clinical and immunological aspects

Antibody detection in Guillain-Brr� syndrome

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