Homology between Klebsiella pneumoniae and human aquaporin-4: no evidence for cross-reactivity in neuromyelitis optica. A study on 114 patients

Jarius, Sven; Wandinger, K. P.; Platzer, Stefan; Wildemann, Brigitte

doi:10.1007/s00415-010-5839-2

Cited by 5 publications

(6 citation statements)

References 17 publications

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“…T cells have also been proposed to be involved in molecular mimicry (e.g. involving bacterial aquaporins), which is currently discussed as a potential trigger of NMO attacks . In addition, a role for glutamate‐mediated excitotoxicity has been discussed. While one study reported that membrane AQP4 in human embryonic kidney (HEK) cells transfected with human AQP4 is endocytosed together with the excitatory amino acid transporter 2 (EAAT2) following incubation with NMO‐IgG in the absence of complement, resulting in disruption of glutamate homeostasis, another study could not confirm these findings in cultures of mouse astrocytes .…”

Section: Immunopathogenesismentioning

confidence: 99%

“…T cells have also been proposed to be involved in molecular mimicry (e.g. involving bacterial aquaporins), which is currently discussed as a potential trigger of NMO attacks .…”

Section: Immunopathogenesismentioning

confidence: 99%

“…T cells have also been proposed to be involved in molecular mimicry (e.g. involving bacterial aquaporins), which is currently discussed as a potential trigger of NMO attacks [160,[181][182][183][184]. (g) In addition, a role for glutamate-mediated excitotoxicity has been discussed.…”

Section: Immunopathogenesismentioning

confidence: 99%

“…AQP4-antibodies are produced mainly by plasma cells in the peripheral blood. The trigger underlying AQP4antibody production is unknown, although molecular mimicry has been suggested [160,[181][182][183][184][212][213][214][215]. By contrast, intrathecal synthesis to an extent detectable by antibody index calculation is very rare [131,136,216,217].…”

Section: Cerebrospinal Fluidmentioning

confidence: 99%

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Neuromyelitis optica: clinical features, immunopathogenesis and treatment

Jarius

Wildemann

Paul

2014

Clinical and Experimental Immunology

311

221

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Neuromyelitis optica: clinical features, immunopathogenesis and treatment OTHER ARTICLES PUBLISHED IN THIS SERIESParaneoplastic neurological syndromes. Clinical and Experimental Immunology 2014, 175: 336-48. Disease-modifying therapy in multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy: common and divergent current and future strategies. Clinical and Experimental Immunology 2014, 175: 359-72. Monoclonal antibodies in treatment of multiple sclerosis. Clinical and Experimental Immunology 2014, 175: 373-84 SummaryThe term 'neuromyelitis optica' ('Devic's syndrome', NMO) refers to a syndrome characterized by optic neuritis and myelitis. In recent years, the condition has raised enormous interest among scientists and clinical neurologists, fuelled by the detection of a specific serum immunoglobulin (Ig)G reactivity (NMO-IgG) in up to 80% of patients with NMO. These autoantibodies were later shown to target aquaporin-4 (AQP4), the most abundant water channel in the central nervous system (CNS). Here we give an up-to-date overview of the clinical and paraclinical features, immunopathogenesis and treatment of NMO. We discuss the widening clinical spectrum of AQP4-related autoimmunity, the role of magnetic resonance imaging (MRI) and new diagnostic means such as optical coherence tomography in the diagnosis of NMO, the role of NMO-IgG, T cells and granulocytes in the pathophysiology of NMO, and outline prospects for new and emerging therapies for this rare, but often devastating condition.

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Section: Immunopathogenesismentioning

confidence: 99%

“…T cells have also been proposed to be involved in molecular mimicry (e.g. involving bacterial aquaporins), which is currently discussed as a potential trigger of NMO attacks .…”

Section: Immunopathogenesismentioning

confidence: 99%

Section: Immunopathogenesismentioning

confidence: 99%

Section: Cerebrospinal Fluidmentioning

confidence: 99%

See 2 more Smart Citations

Neuromyelitis optica: clinical features, immunopathogenesis and treatment

Jarius

Wildemann

Paul

2014

Clinical and Experimental Immunology

311

221

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“…Also, anklyosing spondylitis and Crohn’s disease have been linked to overgrowth of Klebsiella in the gut as a potential causative factor (Rashid and Ebringer, 2012). While the existence of such a mechanism has been suggested for the etiology of NMO (Jarius, et al, 2011) and MS (Kakalacheva and Lunemann, 2011; Varrin-Doyer, et al, 2012), molecular mimicry in the etiology of these diseases has not been documented.…”

Section: Discussionmentioning

confidence: 99%

Aquaporin 4 molecular mimicry and implications for neuromyelitis optica

Vaishnav

Liu

Chapman

et al. 2013

Journal of Neuroimmunology

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Neuromyelitis Optica (NMO) is associated with antibodies to aquaporin 4 (AQP4). We hypothesized that antibodies to AQP4 can be triggered by exposure to environmental proteins. We compared human AQP4 to plant and bacterial proteins to investigate the occurrence of significantly similar structures and sequences. High similarity to a known epitope for NMO-IgG, AQP4(207-232), was observed for corn ZmTIP4-1. NMO and non-NMO serum was assessed for reactivity to AQP4(207-232) and the corn peptide. NMO patient serum showed reactivity to both peptides as well as to plant tissue. These findings warrant further investigation into the role of the environment in NMO etiology.

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The case of the Marquis de Causan (1804): an early account of visual loss associated with spinal cord inflammation

Jarius

Wildemann

2012

J Neurol

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The recent discovery of disease specific and pathogenic autoantibodies in neuromyelitis optica (NMO, Devic's disease) has revived the interest in this intriguing yet often devastating condition. While the history of classic multiple sclerosis has been studied extensively, only very little is known so far about the early history of NMO. Here we discuss a now forgotten report by the famous French anatomist and pathologist Antoine Portal (1742-1832), first physician to Louis XVIII and founding and lifelong president of the Académie Nationale de Médecine. Portal's report, which fascinated some of the most renowned 19th century pioneers in the field of neurology but fell into oblivion later, represents the first account of visual loss in a patient with spinal cord inflammation but no brain pathology in the Western literature known so far--published more than 60 years prior to Thomas Clifford Allbutt's much cited note on a patient with myelitis and a "sympathetic eye disorder".

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Homology between Klebsiella pneumoniae and human aquaporin-4: no evidence for cross-reactivity in neuromyelitis optica. A study on 114 patients

Cited by 5 publications

References 17 publications

Neuromyelitis optica: clinical features, immunopathogenesis and treatment

Neuromyelitis optica: clinical features, immunopathogenesis and treatment

Aquaporin 4 molecular mimicry and implications for neuromyelitis optica

The case of the Marquis de Causan (1804): an early account of visual loss associated with spinal cord inflammation

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