The diagnostic value of sural nerve T cells in chronic inflammatory demyelinating polyneuropathy

Bosboom, W. M. J.; Berg, Leonard H van den; Boer, L. De; Son, Min Jeong; Veldman, H.; Franssen, Hessel; Logtenberg, Ton; Wokke, John H. J.

doi:10.1212/wnl.53.4.837

Cited by 54 publications

(29 citation statements)

References 33 publications

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“…Some forms of vasculitis are thought to result from viral infections, including HIV-1 and hepatitis C (85). While cytotoxic T lymphocytes have been proposed as the mediator of some forms of vasculitis (102), several studies fail to find evidence of T-lymphocyte involvement (24,110). Other forms of vasculitis may derive from the expression of autoantibodies.…”

Section: Clinical Correlation: Vasculitic Neuropathymentioning

confidence: 99%

“…As demyelination and cell death ensue, immune complexes and complement products may be deposited in VN nerves (51,105), leading to more efficient clearing of the debris by activated macrophages. Whether there is an increase in T lymphocytes relative to normal controls is controversial (24,321). If present, T cells may have been attracted to the region primarily as the result of the underlying vasculitis and appear to be infiltrating into the nerve due to ischemic-induced blood-nerve barrier breakdown.…”

Section: C) Evidence For Ischemia-induced Nerve and Immune Changesmentioning

confidence: 99%

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Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Watkins

Maier

2002

Physiological Reviews

655

433

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Chronic pain can occur after peripheral nerve injury, infection, or inflammation. Under such neuropathic pain conditions, sensory processing in the affected body region becomes grossly abnormal. Despite decades of research, currently available drugs largely fail to control such pain. This review explores the possibility that the reason for this failure lies in the fact that such drugs were designed to target neurons rather than immune or glial cells. It describes how immune cells are a natural and inextricable part of skin, peripheral nerves, dorsal root ganglia, and spinal cord. It then examines how immune and glial activation may participate in the etiology and symptomatology of diverse pathological pain states in both humans and laboratory animals. Of the variety of substances released by activated immune and glial cells, proinflammatory cytokines (tumor necrosis factor, interleukin-1, interleukin-6) appear to be of special importance in the creation of peripheral nerve and neuronal hyperexcitability. Although this review focuses on immune modulation of pain, the implications are pervasive. Indeed, all nerves and neurons regardless of modality or function are likely affected by immune and glial activation in the ways described for pain.

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Section: Clinical Correlation: Vasculitic Neuropathymentioning

confidence: 99%

Section: C) Evidence For Ischemia-induced Nerve and Immune Changesmentioning

confidence: 99%

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Watkins

Maier

2002

Physiological Reviews

655

433

View full text Add to dashboard Cite

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“…The presence of nonspecific T cells in the peripheral nerve tissue is in accordance with the finding that T cells are also found in patients with noninflammatory neuropathies and normal controls. 4 Activated nonspecific T cells may help B cells to produce antibodies against peripheral nerve components, thereby inducing activation of either complement or antibodydependent cytolytic cells. 29,30 In CIDP, however, there is not much evidence for a B cell or antibody mediated process.…”

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

confidence: 99%

“…3 In both CIDP and vasculitic neuropathy, increased numbers of T cells in the sural nerve biopsy specimens may indicate a role for T cells in the disease mechanism. [4][5][6] It is currently not clear whether sural nerve T cells, their numbers increased or not, are disease-specific autoreactive T cells, or whether these are attracted nonspecifically to the peripheral nervous tissue.…”

mentioning

confidence: 99%

“…Two patients with CIDP (Patients 1 and 2), three patients with CIAP (Patients 19,20,21), and four autopsy controls (Patients 23 through 26) were selected because of their relatively high number of T cells in the total sural nerve area, as reported in our previous study. 4 Immunohistochemistry. Immunohistochemical staining was performed on 6 m-thick transverse acetone-fixed frozen sections of sural nerves, as well as on sections of tonsil as a positive control.…”

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confidence: 99%

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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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T‐cell cytotoxicity of human Schwann cells: TNFα promotes fasL‐mediated apoptosis and IFNγ perforin‐mediated lysis

Bonetti

Valdo

Ossi

et al. 2003

Glia

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The ability of resident cells to induce apoptosis of invading immune cells is a major regulatory factor operating in immune-privileged tissues, including the nervous system. We investigated the cellular and molecular factors participating in modulation of immune response in peripheral nerves, focusing on two cytotoxic pathways: fas ligand (fasL) and perforin. fasL and perforin expression was found by immunochemistry on Schwann cells (Sc) in nerve biopsies from patients with chronic inflammatory demyelinating polyneuritis and on human Sc cultures. Treatment of Sc with tumor necrosis factor (TNF) alpha and interferon (IFN) gamma upregulated the expression of both molecules. In a coculture model, Sc exposed to TNFalpha or IFN gamma were able to induce both apoptotic and lytic injury of T-lymphocytes. Inactivation of fasL with the neutralizing antibody NOK-2 abolished T-cell apoptosis induced by Sc treated with TNFalpha, but not by Sc treated with IFN gamma. Conversely, T-cell lysis was significantly decreased when IFN gamma-activated Sc were treated with concanamycin A, which inhibited perforin release. At variance with T-lymphocytes, B-cells were less sensitive to cytokine-treated Sc toxicity. Thus, Sc exposed to inflammatory cytokines have the capacity of inducing selective damage of T-lymphocytes and have the potential of regulating the immune response in the peripheral nervous system.

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The diagnostic value of sural nerve T cells in chronic inflammatory demyelinating polyneuropathy

Cited by 54 publications

References 33 publications

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States

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

T‐cell cytotoxicity of human Schwann cells: TNFα promotes fasL‐mediated apoptosis and IFNγ perforin‐mediated lysis

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