Association of neonatal myasthenia gravis with antibodies against the fetal acetylcholine receptor

Garabedian, Béatrice Vernet-der; Lacokova, M; Eymard, B.; Morel, E.; Bach, Jae Hyung

doi:10.1016/0960-8966(94)90109-0

Cited by 10 publications

(17 citation statements)

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“…Another patient, in whom MG was eventually diagnosed, had high titers of anti-AChR antibodies and a similar obstetric history (9). In this paper we define the specificity of anti-AChR antibodies in sera from these two women and from three other mothers whose babies were born with AMC and who had formed part of an earlier survey of neonatal MG (7). The latter three were also positive for anti-AChR but one was asymptomatic.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association of arthrogryposis multiplex congenita with maternal antibodies inhibiting fetal acetylcholine receptor function.

Riemersma¹,

Vincent²,

Beeson³

et al. 1996

J. Clin. Invest.

152

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Section: Introductionmentioning

confidence: 99%

“…A proportion of babies born to MG mothers exhibit transient weakness (neonatal MG) (6), and this is more frequent if the mother's antibody binds preferentially to fetal AChR (7). Occasionally babies have AMC as well as neonatal MG (6,7), suggesting that movement had been severely impaired in utero.…”

Section: Introductionmentioning

confidence: 99%

Association of arthrogryposis multiplex congenita with maternal antibodies inhibiting fetal acetylcholine receptor function.

Riemersma¹,

Vincent²,

Beeson³

et al. 1996

J. Clin. Invest.

152

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“…For example, neonatal lupus, which is clinically characterized by skin eruptions and fatal congenital heart block, is induced by autoAbs against Ro/SSA, Ro/SSB, or U1 ribonuclear protein transferred from mothers affected with Sjögren syndrome or systemic lupus erythematosus (3,4). In addition, maternally transferred autoAbs against acetylcholine receptors can induce the characteristic features of myasthenia gravis in human neonates (5). This suggests that mothers, in experimental animal models, might be able to induce autoimmunity in their offspring.…”

mentioning

confidence: 99%

A Novel Humanized Neonatal Autoimmune Blistering Skin Disease Model Induced by Maternally Transferred Antibodies

Nishie

Sawamura

Natsuga

et al. 2009

The Journal of Immunology

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All mammal neonates receive maternal Abs for protection against pathogenic organisms in the postnatal environment. However, neonates can experience serious adverse reactions if the Abs transferred from the mother recognize self-molecules as autoAgs. In this study, we describe a novel model for autoimmune disease induced by transferred maternal Abs in genetically transformed Ag-humanized mice progeny. Bullous pemphigoid is the most common life-threatening autoimmune blistering skin disease that affects the elderly, in which circulating IgG autoAbs are directed against epidermal type XVII collagen (COL17). We have established a genetically manipulated experimental mouse model in which maternal Abs against human COL17 are transferred to pups whose skin expresses only human and not mouse COL17, resulting in blistering similar to that seen in patients with bullous pemphigoid. Maternal transfer of pathogenic Abs to humanized neonatal mice is a unique and potential experimental system to establish a novel autoimmune disease model.

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“…SCLC cells are derived from the neuroectoderm and secrete a variety of neuropeptides including serotonin and ACTH. The presence of VGCCs in SCLC was first indicated by electrophysiological measurements, and conirmed by showing that depolarization by high K 1 led to an increase in 45 …”

Section: Vgccs Are the Antigenic Target In Lemsmentioning

confidence: 99%

“…Transient weakness occurs during the first days or weeks after birth, the condition responds to AChE inhibitors, and, if recognized, does not present major problems. It is not clear why only some babies develop neonatal MG, but the ability of the mother's serum antibodies to bind to the fetal isoform of the AChR may be a contributory factor [45].…”

Section: Mg and Pregnancymentioning

confidence: 99%

Molecular targets for autoimmune and genetic disorders of neuromuscular transmission

2000

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The neuromuscular junction is the target of a variety of autoimmune, neurotoxic and genetic disorders, most of which result in muscle weakness. Most of the diseases, and many neurotoxins, target the ion channels that are essential for neuromuscular transmission. Myasthenia gravis is an acquired autoimmune disease caused in the majority of patients by antibodies to the acetylcholine receptor, a ligand-gated ion channel. The antibodies lead to loss of acetylcholine receptor, reduced efficiency of neuromuscular transmission and muscle weakness and fatigue. Placental transfer of these antibodies in women with myasthenia can cause fetal or neonatal weakness and occasionally severe deformities. Lambert Eaton myasthenic syndrome and acquired neuromyotonia are caused by antibodies to voltage-gated calcium or potassium channels, respectively. In the rare acquired neuromyotonia, reduced repolarization of the nerve terminal leads to spontaneous and repetitive muscle activity. In each of these disorders, the antibodies are detected by immunoprecipitation of the relevant ion channel labelled with radioactive neurotoxins. Genetic disorders of neuromuscular transmission are due mainly to mutations in the genes for the acetylcholine receptor. These conditions show recessive or dominant inheritance and result in either loss of receptors or altered kinetics of acetylcholine receptor channel properties. Study of these conditions has greatly increased our understanding of synaptic function and of disease aetiology.

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Association of neonatal myasthenia gravis with antibodies against the fetal acetylcholine receptor

Cited by 10 publications

References 0 publications

Association of arthrogryposis multiplex congenita with maternal antibodies inhibiting fetal acetylcholine receptor function.

Association of arthrogryposis multiplex congenita with maternal antibodies inhibiting fetal acetylcholine receptor function.

A Novel Humanized Neonatal Autoimmune Blistering Skin Disease Model Induced by Maternally Transferred Antibodies

Molecular targets for autoimmune and genetic disorders of neuromuscular transmission

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