The role of autoantibody and immune complexes in the pathogenesis of Guillain-Barre syndrome

Cook, Stuart D.; Dowling, Peter C.

doi:10.1002/ana.410090712

Cited by 125 publications

(10 citation statements)

References 54 publications

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“…A number of experiments have shown that cellmediated immunity against an as yet undetermined component of peripheral nerve exists in AIP [57]. Recently interest has centered on the participation of humoral factors (e.g., antibody, immune complexes) in AIP [24], as it has been possible to induce demyelination of peripheral nerve by injecting serum from patients with the disease [38]. Both cellular and humoral components probably contribute.…”

Section: What Is the Mechanism Of Immune Damage?mentioning

confidence: 99%

Neuroimmunology I: Immunoregulation in neurological disease

Weiner

Hauser

1982

Annals of Neurology

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Aberrations in immune function that ultimately result in disease states may involve three aspects of immune regulation: (1) regulatory T cells, which both suppress and induce immune responses; (2) idiotype-antiidiotype networks, which serve as internal regulatory networks during generation of an immune response; and (3) immune response genes, which determine genetic differences in an individual's immune response. Three major diseases of the nervous system, multiple sclerosis, myasthenia gravis, and acute inflammatory polyneuropathy (Guillain-Barré syndrome), are classified as "autoimmune" in nature and may be due to underlying disorders of immunoregulation. In multiple sclerosis there is a loss of suppressor T cells in the peripheral blood during attacks, in myasthenia gravis there are thymic abnormalities and antibodies against the acetylcholine receptor, and in acute inflammatory polyneuropathy, macrophage-mediated destruction of peripheral nerve myelin occurs in the context of sensitized T cells and is usually associated with a preceding viral illness. In each of these diseases the following central questions must be answered: (1) against what antigen (or antigens) of the nervous system is the autoimmune response directed? (2) what is the mechanism of immune damage? and (3) what initiates, or triggers, the autoimmune response?

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Section: What Is the Mechanism Of Immune Damage?mentioning

confidence: 99%

Neuroimmunology I: Immunoregulation in neurological disease

Weiner

Hauser

1982

Annals of Neurology

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“…Although GBS aetiology is unknown, immunological factors are presumably involved [1,2]: the prevailing hypothesis [1,3] considers GBS as an immunopathological reaction triggered by recent exposure to exogenous agents or concomitant diseases (non-specific infec tions, vaccinations, surgical procedures, al lergic phenomena, toxic agents, immunolog ical diseases, etc. ).…”

Section: Introductionmentioning

confidence: 99%

Incidence of the Guillain-Barré Syndrome in Ferrara, Northern Italy, 1981–1987

et al. 1991

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The few incidence estimates on Guillain-Barré syndrome (GBS) in Italy indicate rates lower than the values provided by other previous non-Italian population-based studies. The latter range from 0.6 to 1.9 cases per 100,000 population per year. To verify whether Italy may be considered a low-risk area for GBS we studied the incidence of the disease in Local Health Unit No. 31 (USL 31) of Ferrara, Northern Italy (mean population 180,701 inhabitants) for the years 1981–1987. The annual incidence rates were stable during this period with an average incidence of 1.26 cases per 100,000 population per year. No significant difference was found for urban or rural residence and there was no significant seasonal clustering. In 37.5 % of the series an antecedent infection was recorded within 4 weeks before GBS onset. The survey seems to support the hypothesis of a homogeneous distribution of GBS in space and time and does not support the notion that GBS is less common in Italy than elsewhere.

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“…Although the pathogenesis of GBS is unknown, there is growing evidence to suggest both humoral (Cook & Dowling, 1981;Latov et al, 1981;Vedeler et al, 1982) and cell-mediated (Iqbal et al, 1981) immune mechanisms. Many patients have raised immunoglobulin and acute-phase protein levels, as well as antibodies to peripheral nerve components (Iqbal et al, 1981), however antineuronal antibodies may be found in the sera ofpatients with SLE who do not have evidence of a neuropathy (Bresnihan et al, 1977(Bresnihan et al, , 1979.…”

Section: Discussionmentioning

confidence: 99%