T cell reactivity to P0, P2, PMP-22, and myelin basic protein in patients with Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

Csurhes, Peter A.; Aa, Sullivan; Green, K; Pender, Michael P.; Pa, McCombe

doi:10.1136/jnnp.2004.052282

Cited by 83 publications

(66 citation statements)

References 59 publications

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“…The results of the present study are consistent with an earlier study performed by Ben-Smith et al [5] in which signiWcant proliferative response of peripheral lymphocytes ( T cells) against C. jejuni antigen was found in GBS patients than the controls; interestingly, they also isolated T cells following culture of the nerve tissue. Csurhes et al [6] also performed lymphocyte proliferation assay in patients with In the present study, the results of peripheral cell proliferation in response to PHA from GBS patients and two diVerent groups of controls were similar suggesting that the peripheral cellular response in GBS with preceding C. jejuni infection remains intact.…”

Section: Discussionsupporting

confidence: 68%

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Lymphocyte transformation test detects a response to Campylobacter jejuni antigens in patients with Guillain-Barré syndrome

Nyati

Prasad

Rizwan

et al. 2010

Med Microbiol Immunol

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Guillain-Barré syndrome (GBS) is an immune-mediated polyneuropathy. Campylobacter jejuni-associated gastrointestinal infection is identified as a major precipitating agent of GBS; however, a standard test to diagnose this infection in patients with GBS is lacking. The aim of the present study was to evaluate an outer membrane protein (OMP)-based lymphocyte transformation test (LTT) for the diagnosis of C. jejuni infection in GBS. Forty patients with GBS, age and gender matched 52 healthy controls (HC) and 46 disease controls (DC) were analyzed for C. jejuni infection by culture, polymerase chain reaction (PCR) and LTT. Lymphocytes at concentration of 1 x 10(6)/well isolated from GBS patients and controls were stimulated with 20 microg/ml of C. jejuni OMP, and (3)H-thymidine was incorporated to measure cell proliferation. LTT detected significantly higher C. jejuni infection compared to culture (77.5 vs. 2.5%; P < 0.05) and PCR (77.5 vs. 22.5%; P < 0.05). The cutoff value of lymphocyte proliferation by receiver operating characteristic (ROC) curve of 2.5 had 77.5% sensitivity and 96.5% specificity. Area under ROC curve was 0.92. The mean SI of the cell proliferation for GBS cases was significantly higher than the controls (GBS vs. HC; P < 0.001, GBS vs. DC; P < 0.001). LTT appears to be a sensitive tool for detecting preceding C. jejuni infection in GBS patients with reasonable sensitivity and specificity. It is possible that the activated lymphocytes might play role in the pathogenesis of neuronal damage in GBS.

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Section: Discussionsupporting

confidence: 68%

“…Campylobacter jejuni infection is identiWed as a major triggering agent of GBS, and numerous studies have conWrmed the association between C. jejuni and GBS [4][5][6]. Campylobacter jejuni infection ranges from 25 to 40% in GBS patients throughout the world and usually occurs 1-3 weeks prior to the illness [7].…”

Section: Introductionmentioning

confidence: 99%

Lymphocyte transformation test detects a response to Campylobacter jejuni antigens in patients with Guillain-Barré syndrome

Nyati

Prasad

Rizwan

et al. 2010

Med Microbiol Immunol

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“…It is proposed that activated CD4 T-helper cells bind to specific antigens on myelinproducing Schwann cells or on the myelin sheath itself [11]. This is supported by the observation that T cells reactive to myelin proteins and gangliosides have been found in patients with AIDP [12]. These cells also produce interferon-γ, an important proinflammatory cytokine, in response to stimulation with ganglioside GM1 [13].…”

Section: Acute Inflammatory Demyelinating Polyradiculopathymentioning

confidence: 95%

Guillain-Barré Syndrome: Modern Theories of Etiology

Hardy

Blum

McCombe

et al. 2011

Curr Allergy Asthma Rep

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Guillain-Barré syndrome (GBS) is a classic failure of the immune system with a life-threatening attack upon a critical self-component. The active phase of the disease is short, concordant with the latency of a primary adaptive immune response. Triggers for GBS include infection and (rarely) vaccination; cross-reactivity between infectious and neural epitopes has been well demonstrated, particularly for Campylobacter jejuni and motor axonal forms of GBS in which non-protein gangliosides are antigenic. Most people are probably exposed to a GBS trigger, but only rarely does the disease develop. We propose that GBS illustrates competing determinants of the immune system's decision about whether to mount a response, and that in unlucky affected individuals, co-presentation of cross-reactive antigens with danger signals activating pattern-recognition receptors overcomes normal self-recognition such that a primary response is initiated that attacks the nerve. Then, in most cases of GBS, the response rapidly turns off, and second attacks rarely occur. This suggests active restoration of tolerance, and specific privileged site attributes of nerve and declining danger signals as the trigger wanes may contribute to this restoration. Standard immunosuppression has not been effective in GBS. We suggest this is because immune tolerance is already being restored by the time such therapies are initiated. This in turn suggests that improvements in GBS outcomes are likely to come from better protection of the nerve cells under attack while normal resumption of tolerance is permitted to proceed rather than exploring more aggressive immunosuppressive approaches.

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“…More recently, patients with increased anti-GM1 T cell reactivity were significantly less severe than those without such reactivity. This raises the possibility that increased GM1 specific T cell reactivity and its related cytokine might have an immuneregulatory or neuro-protective role [173].…”

Section: Therapies On Cytokines In Ean and Gbsmentioning

confidence: 99%

The role of cytokines in Guillain–Barré syndrome

Zhu

2010

J Neurol

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Cytokines play an important role in the pathogenesis of autoimmune diseases including Guillain-Barré syndrome (GBS) and its animal model experimental autoimmune neuritis (EAN). In this article, we reviewed the current knowledge of the role of cytokines such as TNF-α, IFN-γ, IL-1β, IL-6, IL-12, IL-18, IL-23, IL-17, IL-10, IL-4 and chemokines in GBS and EAN as unraveled by studies both in the clinic and the laboratory. However, these studies occasionally yield conflicting results, highlighting the complex role that cytokines play in the disease process. Efforts to modulate cytokine function in GBS and other autoimmune disease have shown efficiency indicating that cytokines are important therapeutic targets.

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T cell reactivity to P0, P2, PMP-22, and myelin basic protein in patients with Guillain-Barre syndrome and chronic inflammatory demyelinating polyradiculoneuropathy

Cited by 83 publications

References 59 publications

Lymphocyte transformation test detects a response to Campylobacter jejuni antigens in patients with Guillain-Barré syndrome

Lymphocyte transformation test detects a response to Campylobacter jejuni antigens in patients with Guillain-Barré syndrome

Guillain-Barré Syndrome: Modern Theories of Etiology

The role of cytokines in Guillain–Barré syndrome

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