Immunopathogenesis and treatment of the guillain–barré syndrome—part II

Hartung, Hans‐Peter; Toyka, Klaus V.; Pollard, John D.; Harvey, Graham K.

doi:10.1002/mus.880180203

Cited by 181 publications

(57 citation statements)

References 106 publications

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“…Up to 30% of cases are preceded by an infection with the Gram-negative bacterium Campylobacter jejuni [2], a leading cause of acute gastroenteritis in humans [3]. Several studies have suggested that immune recognition of cross-reacting epitopes on antigens common to C. jejuni and peripheral nerve myelin might provide a possible mechanism by which an autoreactive response leads to demyelination [1,4]. Support for a such an autoimmune etiology comes from recent reports of structural similarity between the lipopolysaccharide (LPS) of C. jejuni strains isolated from GBS patients and the peripheral nerve gangliosides GM1, GQ1b and GD1a [5,6].…”

Section: Introductionmentioning

confidence: 99%

Stimulation of peripheral blood lymphocytes with Campylobacter jejuni generates a γδ T cell response in patients with Guillain–Barré syndrome

Ben-Smith¹,

Goodall

Gaston

et al. 1997

Clinical and Experimental Immunology

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SUMMARYIn three patients whose Guillain-Barré syndrome (GBS) was preceded by gastrointestinal infection due to Campylobacter jejuni, gd T cells were generated from peripheral blood in response to in vitro stimulation with C. jejuni. In one of the patients, where a diagnostic sural nerve biopsy was performed, gd T cells were also isolated following culture of the nerve tissue. Studies with healthy volunteers and C. jejuni gastroenteritis patients also showed preferential enrichment for gd T cells in peripheral blood cells stimulated with C. jejuni, although the response was significantly lower than that seen in GBS patients. In two out of three GBS patients and all of the controls, gd T cell receptor (TCR) gene usage was shown to be Vg9/Vd2 + . In the GBS patient where nerve-infiltrating gd T cells were isolated, these and C. jejuni-specific peripheral blood cells had similar TCR gene usage, predominantly consisting of Vg5/Vd1 + cells. Sequencing the Vd1 products from nerve and peripheral blood showed similarities in CDR3 length, but the single Vd1 sequence obtained from nerve was not identified in peripheral blood. These results suggest that the generation of gd T cells is part of a normal immune response to C. jejuni, which, in patients with GBS, may contribute to the pathogenesis of their inflammatory neuropathy.

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Section: Introductionmentioning

confidence: 99%

Stimulation of peripheral blood lymphocytes with Campylobacter jejuni generates a γδ T cell response in patients with Guillain–Barré syndrome

Ben-Smith¹,

Goodall

Gaston

et al. 1997

Clinical and Experimental Immunology

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“…Thus, other mechanisms, besides the M-protein acting as antibodies, may be operating. In another demyelinating polyneuropathy, the Guillain-Barré syndrome (GBS), T cell-mediated mechanisms are proposed ( [11,12]; Dahle et al, data to be published). There are some reports suggesting that T cells also may be involved in the pathogenesis of polyneuropathy associated with monoclonal gammopathy.…”

Section: Introductionmentioning

confidence: 99%

Th1-like responses to peptides from peripheral nerve myelin proteins in patients with polyneuropathy associated with monoclonal gammopathy

Ekerfelt¹,

Ernerudh²,

Vrethem³

1997

Clinical and Experimental Immunology

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SUMMARYPolyneuropathy associated with monoclonal gammopathy is usually regarded as an immune-mediated disorder with autoantibody activity against myelin glycoproteins. The pathogenic mechanisms are, however, not fully understood. Several reports have indicated an additional involvement of T cells. We investigated the occurrence of myelin-specific T cells as well as their functional characteristics. Cytokine responses generated after stimulation of peripheral blood mononuclear cells with selected peptides of myelin proteins P0 and P2 were investigated with an ELISPOT method. Three P0 peptides caused significantly elevated levels of interferon-gamma (IFN-g)-secreting cells in patients with polyneuropathy associated with monoclonal gammopathy (n ¼ 8) compared with controls (n ¼ 8), whereas none of the peptides caused elevated levels of IL-4-secreting cells. Patients with nonimmunological types of neuropathy (n ¼ 4) did not reveal any cytokine responses to myelin peptides. Our results indicate that a Th1-like response against myelin proteins occurs in polyneuropathy associated with monoclonal gammopathy.

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“…Glukokortikoide zeigen beim GBS keinen Effekt (17,18). Bei Übergang in die chronische GBSForm, die chronisch-inflammatorisch demyelinisierende Polyradikuloneuropathie (CIDP) und bei der relapsierenden Form sind Glukokortikoide indiziert (initial 1-1,5 mg/kg KG, meist 80-120 mg/die), auch die Plasmapherese kommt zum Einsatz (38).…”

Section: Primär Demyelinisierende Polyneuropathien (Immunvermittelt)unclassified

Polyneuropathy - Treatment

Schlotter-Weigel¹,

Pongratz²

2002

Dtsch med Wochenschr

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Glossar: AMA = antimitochrondriale AK; ANA = antinukleäre Antikörper; ANCA = antineutrophile cytoplasmatische Antikörper; AK = Antikörper; CIDP = chronische inflammatorisch-demyelinisierende Polyradikulopathie; ds-DNS-AK = doppelsträngige DNSAntikörper; GBS = Guillain-Barré-Syndrom; GM1-/GM2-/GQ1b-/ Gd1a-AK=Gangliosid AK; HNPP=Hereditäre Neuropathie mit Neigung zu Druckparesen; IVIG = intravenöse Immunglobulingabe; MAG = Myelin-assoziiertes Glykoprotein; MGUS = monoklonale Gammopathie unbestimmter Signifikanz; MMN = Multifokale motorische Neuropathie; MRT = Magnetresonanztomographie; PNP = Polyneuropathie; PMP = peripheres Myelin-Protein; SGPG = Sulfoglucuronyl-Paragloboside Primär demyelinisierende Polyneuropathien (immunvermittelt)Guillain-Barré-Syndrom (und Unterformen) / chronische inflammatorisch-demyelinisierende Polyradikulopathie / Paraproteinämien Die intravenöse hochdosierte Immunglobulingabe (IVIG) mit 0,4 g/kg KG über 5 Tage wird beim GBS als nicht-invasive Therapieform meist bevorzugt und ist in ihrer Wirkung der Plasmapherese gleichzusetzen (37). Glukokortikoide zeigen beim GBS keinen Effekt (17,18). Bei Übergang in die chronische GBSForm, die chronisch-inflammatorisch demyelinisierende Polyradikuloneuropathie (CIDP) und bei der relapsierenden Form sind Glukokortikoide indiziert (initial 1-1,5 mg/kg KG, meist 80-120 mg/die), auch die Plasmapherese kommt zum Einsatz (38). Die positive Wirkung von IVIG bei CIDP wurde in mehreren Studien belegt (39). Tritt unter diesen Therapien keine Besserung ein, kommen zusätzlich immunsuppressive Substanzen wie Azathioprin, Methotrexat und Cyclophosphamid zum Einsatz. Eine Studie (11) zeigte jedoch keinen weiteren Nutzen durch Gabe von Azathioprin in Kombination mit Glukokortikoiden. In Einzelfällen konnte eine Stabilisierung oder Besserung durch Gabe von Cyclosporin A erzielt werden in einer Anfangsdosis von 3-5 mg/kg KG/die (24). CIDP-Patienten mit proximalen und distalen Paresen scheinen von einer Glukokortikoidgabe zu profitieren, unabhängig ob es sich um eine CIDP oder eine CIDP-MGUS handelt (2). Bei Paraproteinämien bei zugrunde liegendem Plasmozytom und M. Waldenström wird die jeweilige Grunderkrankung therapiert. Plasmapherese kann effektiv sein bei . Patienten mit monoklonaler IgMGammopathie mit oder ohne MAG-AK, können von intensivierten immunmodulierenden Therapien profitieren, wie einige Untersuchungen gezeigt haben: unter anderem von Plasmapherese (16), Plasmapherese plus iv-Cyclophosphamid (3), Plasmapherese plus Chlorambucil (32), hochdosierter intravenöse Immunglobulingabe (IVIG) (7), der Gabe von alpha-Interferon (25). Nicht immer spricht diese Neuropathie auf eine zytostatische Therapie an (29). Multifokale Motorische NeuropathieViele Autoren berichteten über die Behandlung mit Glukokortikoiden allein (36) oder in Kombination mit Plasmapherese oder immunsuppressiven Substanzen (14). Nur bei wenigen Patienten wurde damit eine Besserung erzielt (8), wesentlich mehr zeigten sogar eine klinische Verschlechterung (10). Seit 1992 ist bekannt, dass dies...

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Immunopathogenesis and treatment of the guillain–barré syndrome—part II

Cited by 181 publications

References 106 publications

Stimulation of peripheral blood lymphocytes with Campylobacter jejuni generates a γδ T cell response in patients with Guillain–Barré syndrome

Stimulation of peripheral blood lymphocytes with Campylobacter jejuni generates a γδ T cell response in patients with Guillain–Barré syndrome

Th1-like responses to peptides from peripheral nerve myelin proteins in patients with polyneuropathy associated with monoclonal gammopathy

Polyneuropathy - Treatment

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