Title: Antibodies Affecting Ion Channel Function in Acquired Neuromyotonia, in Seropositive and Seronegative Myasthenia Gravis, and in Antibody‐mediated Arthrogryposis Multiplex Congenita
Abstract: Annals of the New York Academy of SciencesVolume 841, Issue 1 p. 482-496 Antibodies Affecting Ion Channel Function in Acquired Neuromyotonia, in Seropositive and Seronegative Myasthenia Gravis, and in Antibody-mediated Arthrogryposis Multiplex Congenita ANGELA VINCENT, ANGELA VINCENT Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorLESLIE JACOBSON, LESLIE JACOBSON Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorPAUL PLESTED, PAUL PLESTED Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorAGATA POLIZZI, AGATA POLIZZI Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorTERESA TANG, TERESA TANG Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorSIETSKE RIEMERSMA, SIETSKE RIEMERSMA Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorCLAIRE NEWLAND, CLAIRE NEWLAND Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorSARA GHORAZIAN, SARA GHORAZIAN Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorJEREMY FARRAR, JEREMY FARRAR Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorCAL MACLENAN, CAL MACLENAN Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorNICHOLAS WILLCOX, NICHOLAS WILLCOX Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorDAVID BEESON, DAVID BEESON Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorJOHN NEWSDOM-DAVIS, JOHN NEWSDOM-DAVIS Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this author ANGELA VINCENT, ANGELA VINCENT Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorLESLIE JACOBSON, LESLIE JACOBSON Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorPAUL PLESTED, PAUL PLESTED Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorAGATA POLIZZI, AGATA POLIZZI Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorTERESA TANG, TERESA TANG Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorSIETSKE RIEMERSMA, SIETSKE RIEMERSMA Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorCLAIRE NEWLAND, CLAIRE NEWLAND Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorSARA GHORAZIAN, SARA GHORAZIAN Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorJEREMY FARRAR, JEREMY FARRAR Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorCAL MACLENAN, CAL MACLENAN Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorNICHOLAS WILLCOX, NICHOLAS WILLCOX Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorDAVID BEESON, DAVID BEESON Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this authorJOHN NEWSDOM-DAVIS, JOHN NEWSDOM-DAVIS Neurosciences Group; Institute of Molecular Medicine; John Radcliffe Hospital; University of Oxford; Headington, Oxford OX3 9DS, United KingdomSearch for more papers by this author First published: 07 February 2006 https://doi.org/10.1111/j.1749-6632.1998.tb10968.xCitations: 25Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat REFERENCES 1 Newsom-Davis, J. & K. R. Mills. 1993. Immunological associations of acquired neuromyotonia (Isaacs' syndrome): report of five cases and literature review. Brain 116: 453–469. 2 Sinha, S., J. Newsom-Davis, K. Miles et al. 1991. Autoimmune aetiology for acquired neuromyotonia (Isaacs' syndrome). Lancet 338: 75–77. 3 Bady, B., G. Chauplannaz, C. Vial et al. 1991. Autoimmune aetiology for acquired neuromyotonia. Lancet 338: 1330. 4 Wintzen, A. R., J. G. Van Dijk & A. BRAND. 1994. Neuromyotonia with early response to plasmapheresis associated with proximal action myoclonus with late response to plasmapheresis. Muscle Nerve 17(suppl. 1): S221. 5 Shillito, P., P C. Molenaar, A. Vincent et al. 1995. Acquired neuromyotonia: evidence for autoantibodies against K+ channels of peripheral nerves. Ann. Neurol. 38: 714–722. 6 Hart, I. K., C. Waters, A. Vincent et al. 1997. Autoantibodies detected to expressed K+ channels are implicated in neuromyotonia (Isaacs' syndrome). Ann. Neurol. 41: 238–246. 7 Halbach, M., V. Homberg & H-J. Freund. 1987. Neuromuscular, autonomic, and central cholinergic hyperactivity associated with thymoma and acetylcholine receptor-binding antibody. J. Neurol. 234: 433–436. 8 Vincent, A., P. J. Whiting, M. Schluep et al. 1987. Antibody heterogeneity and specificity in myasthenia gravis. Ann. N.Y. Acad. Sci. 505: 106–120. 9 Tzartos, S. J., T. Barkas, M. T. Cung et al. 1991. The main immunogenic region of the acetylcholine receptor: structure and role in myasthenia gravis. Autoimmunity 8: 259–270. 10 Vincent, A. & J. Newsom-Davis. 1982. Acetylcholine receptor antibody characteristics in myasthenia gravis. 1. Patients with generalized myasthenia or disease restricted to ocular muscles. Clin. Exp. Immunol. 49: 257–265. 11 Beeson, D., M. Amar, I. Bermudez et al. 1996. Stable high level expression of the adult subtype of human muscle acetylcholine receptor in the TE671 cell line following transfection with cDNA encoding the ɛ subunit. Neurosci. Lett. 207: 57–60. 12 Geuder, K. I., A. Marx, V. Witzemann et al. 1992. Genomic organization and lack of transcription of the nicotinic acetylcholine receptor subunit genes in myasthenia gravis-associated thymoma. Lab. Invest. 66: 452–458. 13 Kaminski, H. J., R. A. Fenstermaker, F. W. Abdul Karim et al. 1993. Acetylcholine receptor subunit gene expression in thymic tissue. Muscle Nerve 16: 1332–1337. 14 Horton, R. M., A. A. Manfredi & B. M. Conti-Tronconi. 1993. The "embryonic" gamma subunit of the nicotinic acetylcholine receptor is expressed in adult extraocular muscle. Neurology 43(5): 983–985. 15 Kaminski, H., L. Kusner & C. Block. 1996. Expression of acetylcholine receptor isoforms at extraocular endplates. Invest. Ophthalmol. Visual Sci. 321: 406–411. 16 MacLennan, C., D. Beeson, A-M. Buijs et al. 1997. Acetylcholine receptor expression in human extraocular muscles and their susceptibility to myasthenia gravis. Ann. Neurol. 41: 423–431. 17 Kaminski, H. J., & U. L. Ruff. 1997. Ocular muscle involvement by myasthenia gravis. Editorial. Ann. Neurol. 41: 419–420. 18 Beeson, D., L. Jacobson, J. Newsom-Davis et al. 1996. A transfected human muscle cell line expressing the adult subtype of the human muscle acetylcholine receptor for diagnostic assays in myasthenia gravis. Neurology 47: 1552–1555. 19 Vincent, A. 1980. Immunology of acetylcholine receptors in relation to myasthenia gravis. Physiol. Rev. 60: 756–824. 20 Whiting, P. J., A. Vincent & J. Newsom-Davis. 1986. Myasthenia gravis: monoclonal antihuman acetylcholine receptor antibodies used to analyze antibody specificities and responses to treatment. Neurology 36: 612–617. 21 Tzartos, S. J., & J. L. Lindstrom. 1980. Monoclonal antibodies to probe acetylcholine receptor structure: localization of the main immunogenic region and detection of similarities between subunits. Proc. Natl. Acad. Sci. U.S.A. 77: 755–759. 22 Heidenreich, F., A. Vincent, A. Roberts et al. 1988. Epitopes on human acetylcholine receptor defined by monoclonal antibodies and myasthenia gravis sera. Autoimmunity 1: 285–297. 23 Farrar, J., S. Portolano, N. Willcox et al. 1997. Diverse Fabs specific for acetylcholine receptor epitopes from a myasthenia gravis thymus combinatorial library. Int. Immunol. In press. 24 Graus, Y. F., M. H. De Baets, P. W. H. Parren et al. 1997. Human anti-nicotinic acetylcholine receptor recombinant Fab fragments isolated from thymus-derived phage display libraries from myasthenia gravis patients reflect predominant specificities in serum and block the action of pathogenic serum antibodies. J. Immunol. 158: 1919–1929. 25 Drachman, D. B., & A. J. Coulombre. 1961. Experimental clubfoot and arthrogryposis multiplex congenita. Lancet ii: 523. 26 Vernet Der Garabedian, B., M. Lacokova, B. Eymard et al. 1994. Association of neonatal myasthenia gravis with antibodies against the fetal acetylcholine receptor. J. Clin. Invest. 94: 555–559. 27 Hall, J. G. 1990. Arthrogryposes (multiple congenital contractures). In Principles and Practice of Medical Genetics. Churchill Livingstone. New York. 28 Vincent, A., C. Newland, L. Brueton et al. 1995. Arthrogryposis multiplex congenita with maternal autoantibodies specific for a fetal antigen. Lancet 346: 24–25. 29 Barnes, P., D. Kanabar, L. Brueton et al. 1994. Recurrent congenital arthrogryposis leading to a diagnosis of myasthenia gravis in an initially asymptomatic mother. Neuromusc. Dis. 5: 59–65. 30 Riemersma, S., A. Vincent, D. Beeson et al. 1996. Association of arthrogryposis multiplex congenita with maternal antibodies inhibiting fetal acetylcholine receptor function. J. Clin. Invest. 98: 2358–2363. 31 Sanders, D. B., I. Andrews, J.F. Howard et al. 1997. Seronegative myastenia gravis. Neorology 48(suppl.5): S40–S45. 32 Vincent, A., Z. Lt. A. Hart et al. 1993. Seronegative myasthenia gravis:evidence for plasma factor(s) interfering with acetycholine receptor function. Ann. N.Y. Acad. Sci. 681: 529–538. 33 Mossman, S., A. Vincent & J. Newsom-Davis. 1986. Myasthenia gravis without acetylcholine-receptor antibody: a distict disease entity. Lancet i: 116–119. 34 Burges, J., D. W. Wray, S. Pizzighella et al. 1990. A myasthenia gravis plasma immunoglobulin reduces miniature endplate potentials at human endplates in vitro. Muscle Nerve 13: 407–413. 35 Yamamoto, T., A. Vincent, T. A. Ciulla et al. 1991. Seronegative myasthenia gravis: a plasma factor inhibiting agonist-induced acetylcholine receptor function copurifies with IgM. Ann. Neurol. 30: 550–557. 36 Barrett-Jolley, R., N. Byrne, A. Vincent et al. 1994. Seronegative myasthenia gravis plasmas reduce acetylcholine-induced currents in TE671 cells. Pflügers Arch. 428: 492–498. 37 Li, Z., N. Forester & A. Vincent. 1993. Modulation of acetylcholine receptor function in TE671 (rhabdomyosarcoma) cells by non-AChR ligands; a role in seronegative myasthenia gravis?. J. Neuroimmunol. 64: 179–184. 38 Huganir, R. L., & K. Miles. 1989. Protein phosphorylation of nicotinic acetylcholine receptors. Crit. Rev. Biochem. 24: 183–215. Citing Literature Volume841, Issue1MYASTHENIA GRAVIS AND RELATED DISEASES: DISORDERS OF THE NEUROMUSCULAR JUNCTIONMay 1998Pages 482-496 ReferencesRelatedInformation
Publication Year: 1998
Publication Date: 1998-05-01
Language: en
Type: review
Indexed In: ['crossref', 'pubmed']
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Cited By Count: 41
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