Anti-neuroblastoma antibodies in myasthenia gravis: clinical and immunological correlations

Müller, Kiti

doi:10.1016/0022-510x(89)90196-2

Cited by 8 publications

(3 citation statements)

References 43 publications

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“…(4) Auto-antibodies against neuroblastoma cell lines, which are often used to determine antibodies against neural antigenic targets, are present in 40 -60% of MG patients. However, low titers have also been observed in more than 10% of healthy individuals [201][202][203]. The presence of these antibodies provides evidence for autoimmunization against antigens of neural origin in MG. (5) Anti-thymus antibodies have been found in 45% of MG patients with a normal or hyperplastic thymus [204].…”

Section: Rarely Studied Auto-antibodies In Mgmentioning

confidence: 96%

The auto-antigen repertoire in myasthenia gravis

Vrolix¹,

Fraussen²,

Molenaar³

et al. 2010

Autoimmunity

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Myasthenia Gravis (MG) is an antibody-mediated autoimmune disorder affecting the postsynaptic membrane of the neuromuscular junction (NMJ). MG is characterized by an impaired signal transmission between the motor neuron and the skeletal muscle cell, caused by auto-antibodies directed against NMJ proteins. The auto-antibodies target the nicotinic acetylcholine receptor (nAChR) in about 90% of MG patients. In approximately 5% of MG patients, the muscle specific kinase (MuSK) is the auto-antigen. In the remaining 5% of MG patients, however, antibodies against the nAChR or MuSK are not detectable (idiopathic MG, iMG). Although only the anti-nAChR and anti-MuSK auto-antibodies have been demonstrated to be pathogenic, several other antibodies recognizing self-antigens can also be found in MG patients. Various auto-antibodies associated with thymic abnormalities have been reported, as well as many non-MG-specific auto-antibodies. However, their contribution to the cause, pathology and severity of the disease is still poorly understood. Here, we comprehensively review the reported auto-antibodies in MG patients and discuss their role in the pathology of this autoimmune disease.

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Section: Rarely Studied Auto-antibodies In Mgmentioning

confidence: 96%

The auto-antigen repertoire in myasthenia gravis

Vrolix¹,

Fraussen²,

Molenaar³

et al. 2010

Autoimmunity

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“…auto-antibodies against neuroblastoma cell lines, which are often used to determine antibodies against neural antigenic targets, are present in 40-60% of MG patients. However, low titers have also been observed in more than 10% of healthy individuals (Muller, 1989;Muller and Andersson, 1984;Muller et al, 1991). The presence of these antibodies provides evidence for autoimmunization against antigens of neural origin in MG; 5.)…”

Section: Rarely Studied Auto-antibodies In Mgmentioning

confidence: 99%

“…No. (Meager et al, 1997); (Meager et al, 1999); (Buckley et al, 2001); ; ; (Yoshikawa et al, 2006) 29 Heat shock protein 30-80% -/ +/-Chaperone IC (Munakata et al, 2008); (Astarloa and Martinez Castrillo, 1996) 30 Muller, 1989;Muller and Andersson, 1984;Muller et al, 1991) 34 Thymus 40-75% / Lymphoid organ / (Hazama et al, 1989); (Safar et al, 1991) 35 IC (Sasaki et al, 2001); (Gordon et al, 1992) M: Membrane protein, IC: intracellular protein, EC: extracellular protein, S: secreted protein, Ep: epinephrine, NE: norepinephrine, HT: Hashimoto"s thyroiditis, GD: Graves"s disease, EC: excitation-contraction, NAT: Neonatal alloimmune thrombocytopenie, AAG: autoimmune autonomic ganglionopathy, LEMS: Lambert-Eaton myasthenic syndrome, TSH: thyroid stimulating hormone (Meager et al, 1997); (Meager et al, 1999); (Buckley et al, 2001); ; ; (Yoshikawa et al, 2006 (Meager et al, 1997); (Meager et al, 1999); (Buckley et al, 2001); ; ; (Yoshikawa et al, 2006) -/ +/-Chaperone IC (Munakata et al, 2008); (Astarloa and Martinez Castrillo, 1996 (Sasaki et al, 2001); (Gordon et al, 1992) llular protein, EC: extracellular protei...…”

Section: -40%mentioning

confidence: 99%

The autoreactive B cell response in myasthenia gravis

Vrolix¹

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