Immunological investigation of chronic inflammatory demyelinating polyradiculoneuropathy

Melendez‐Vasquez, Carmen V.; Redford, Jane; Choudhary, Pratik; Gray, I. A.; Maitland, Philip; Gregson, N. A.; Smith, Kenneth J.; Hughes, Richard

doi:10.1016/s0165-5728(96)00189-0

Cited by 106 publications

(76 citation statements)

References 56 publications

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“…29,30 In CIDP, however, there is not much evidence for a B cell or antibody mediated process. [31][32][33] Another function of nonspecific T cells may be to increase the blood-nerve barrier permeability and recruit macrophages, as has been hypothesized in experimental model of inflammatory neuropathy in Lewis rats. 34,35 Local accumulation of high numbers of non-neural T cells induced severe axonal degeneration and conduction failure, while lower numbers induced conduction block and mild demyelination.…”

Section: Comparison Of V␤ Utilization In Sural Nerve Biopsy Specimensmentioning

confidence: 99%

Sural nerve T-cell receptor Vβ gene utilization in chronic inflammatory demyelinating polyneuropathy and vasculitic neuropathy

Bosboom

Berg²,

Mollee³

et al. 2001

Neurology

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Article abstract-Objective: To investigate the utilization of T-cell receptor (TCR) variable (V) regions in infiltrates of sural nerve biopsies of patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and vasculitic neuropathy. Background: The presence of infiltrating T lymphocytes in sural nerve biopsies may suggest a T cell-mediated immune mechanism in the pathogenesis of CIDP and vasculitic neuropathy. Patients and methods: The utilization of TCR V␤ regions in sural nerves of 13 patients with CIDP and five patients with vasculitic neuropathy was determined by immunohistochemistry, reverse-transcription PCR, and nucleotide sequence analysis. These techniques were also applied in four patients with chronic idiopathic axonal polyneuropathy (CIAP) who acted as noninflammatory controls, and in five autopsy controls. Results: The TCR V␤ utilization of infiltrating T cells in sural nerves of patients with CIDP, vasculitic neuropathy, and noninflammatory controls is heterogeneous. A dominant TCR V␤ utilization was not found in any of the patients or controls. Conclusion: There is no evidence for the presence of clonally expanded T cells in sural nerves of patients with CIDP and vasculitic neuropathy.

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Section: Comparison Of V␤ Utilization In Sural Nerve Biopsy Specimensmentioning

confidence: 99%

Sural nerve T-cell receptor Vβ gene utilization in chronic inflammatory demyelinating polyneuropathy and vasculitic neuropathy

Bosboom

Berg²,

Mollee³

et al. 2001

Neurology

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“…Secondly, the second episode was controlled successfully with corticosteroid pulse therapy, which is well known to be ineffective in GBS. Although one-fourth to one-third of CIDP patients report a history of illness in the preceding weeks before the onset of CIDP, most of the reported illnesses are nonspecific upper respiratory infections 2 and, unlike GBS, no specific infections have ever been confirmed to be associated with the development of CIDP. Thus, the association between HAV and the onset of A-CIDP in the present case is especially noteworthy.…”

Section: Discussionmentioning

confidence: 99%

Acute-onset chronic inflammatory demyelinating polyneuropathy following hepatitis A virus infection

Jung

Kim

Min

et al. 2017

Ann Clin Neurophysiol

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“…Studies looking for antibodies to gangliosides have been unrewarding in CIDP in contrast to MMN. 18 Antibodies are not believed to, by themselves, produce demyelination as they are unable to penetrate the blood-nerve barrier unless it is already permeable. There is evidence that a T-cell response is also involved.…”

Section: Dovepressmentioning

confidence: 99%

Overview of the pathogenesis and treatment of chronic inflammatory demyelinating polyneuropathy with intravenous immunoglobulins

Mahdi-Rogers

Rajabally²

2010

BTT

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Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired heterogeneous disorder of immune origin affecting the peripheral nerves, causing motor weakness and sensory symptoms and signs. The precise pathophysiology of CIDP remains uncertain although B and T cell mechanisms are believed to be implicated. Intravenous immunoglobulins (IVIg) have been shown in a number of trials to be an effective treatment for CIDP. IVIg is thought to exert its immunomodulatory effects by affecting several components of the immune system including B-cells, T-cells, macrophages and complement. This article provides an overview of the pathogenesis of CIDP and of its treatment with IVIg.

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Immunological investigation of chronic inflammatory demyelinating polyradiculoneuropathy

Cited by 106 publications

References 56 publications

Sural nerve T-cell receptor Vβ gene utilization in chronic inflammatory demyelinating polyneuropathy and vasculitic neuropathy

Sural nerve T-cell receptor Vβ gene utilization in chronic inflammatory demyelinating polyneuropathy and vasculitic neuropathy

Acute-onset chronic inflammatory demyelinating polyneuropathy following hepatitis A virus infection

Overview of the pathogenesis and treatment of chronic inflammatory demyelinating polyneuropathy with intravenous immunoglobulins

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