Marta Pedreño1, Maria Sepúlveda2, Thais Armangué3, Lidia Sabater1, Eugenia Martínez-Hernandez2, Georgina Arrambide4, Yolanda Blanco2, Sara Llufriu2, Elena H Martínez-Lapiscina2, Patricia Mulero4, Nuria Sola-Valls2, Raquel Ruiz-García5, Mar Tintoré4, Josep Dalmau6, Francesc Graus2, Albert Saiz7. 1. Neuroimmunology Program, Institut d' Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain. 2. Neuroimmunology Program, Institut d' Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Unitat de Neuroimmunologia-Esclerosi múltiple, Servei de Neurología, Hospital Clinic, and Universitat de Barcelona, Barcelona, Spain. 3. Neuroimmunology Program, Institut d' Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Unitat de Neuroimmunologia-Esclerosi múltiple, Servei de Neurología, Hospital Clinic, and Universitat de Barcelona, Barcelona, Spain; Pediatric Neuroimmunology Unit, Sant Joan de Deu Children's Hospital, University of Barcelona, Spain. 4. Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya, (Cemcat), Vall d'Hebron Institut de Recerca, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain. 5. Servicio de Inmunología, Centro de Diagnóstico Biomédico, Hospital Clinic of Barcelona, Barcelona, Spain. 6. Neuroimmunology Program, Institut d' Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Unitat de Neuroimmunologia-Esclerosi múltiple, Servei de Neurología, Hospital Clinic, and Universitat de Barcelona, Barcelona, Spain; Department of Neurology, University of Pennsylvania, Philadelphia, PA; Catalan Institution for research and Advanced Studies (ICREA), Barcelona, Spain. 7. Neuroimmunology Program, Institut d' Investigació Biomèdica August Pi i Sunyer (IDIBAPS), Barcelona, Spain; Unitat de Neuroimmunologia-Esclerosi múltiple, Servei de Neurología, Hospital Clinic, and Universitat de Barcelona, Barcelona, Spain. Electronic address: asaiz@clinic.cat.
Abstract
OBJECTIVE: To determine the frequency and relevance of IgM, and IgA antibodies against myelin oligodendrocyte glycoprotein (MOG) in MOG-IgG-associated disease. METHODS: Evaluation of IgM, and IgA MOG antibodies in serum of 120 patients with MOG-IgG (53 pediatric and 67 adults), and 114 patients with seronegative-MOG-IgG (35 children with first demyelinating syndrome, 20 adults with clinically isolated syndrome, and 59 adults with other diseases). Antibodies were examined by cell-based assays. RESULTS: IgM or IgA MOG antibodies were identified in 23/120 (19%) patients with MOG-IgG (13/53 [24.5%] pediatric, and 10/67 [15%] adult patients), and 2/114 (1.7%) patients with seronegative-MOG-IgG (2/35 [5.7%] pediatric patients). Of the 25 patients, 14 had IgA, 9 IgM, and 2 both antibodies. Fourteen of the 15 (93%) children with IgM (4), IgA (9), or both (2) had acute demyelinating encephalomyelitis (ADEM), and 7 of the 10 (70%) adults with IgM (5) or IgA (5) had optic neuritis at onset. At the last follow-up, the final diagnoses remained as ADEM in 14 (100%) children and optic neuritis in 6 (86%) adults. The outcome was not different between patients with or without additional classes of antibodies. CONCLUSION: Coexisting IgM and IgA antibodies occurs in 19% of children and adult patients with MOG-IgG-associated disease. The presence of these antibodies does not seem to play a relevant clinical role in the disorder.
OBJECTIVE: To determine the frequency and relevance of IgM, and IgA antibodies against myelin oligodendrocyte glycoprotein (MOG) in MOG-IgG-associated disease. METHODS: Evaluation of IgM, and IgA MOG antibodies in serum of 120 patients with MOG-IgG (53 pediatric and 67 adults), and 114 patients with seronegative-MOG-IgG (35 children with first demyelinating syndrome, 20 adults with clinically isolated syndrome, and 59 adults with other diseases). Antibodies were examined by cell-based assays. RESULTS: IgM or IgA MOG antibodies were identified in 23/120 (19%) patients with MOG-IgG (13/53 [24.5%] pediatric, and 10/67 [15%] adult patients), and 2/114 (1.7%) patients with seronegative-MOG-IgG (2/35 [5.7%] pediatric patients). Of the 25 patients, 14 had IgA, 9 IgM, and 2 both antibodies. Fourteen of the 15 (93%) children with IgM (4), IgA (9), or both (2) had acute demyelinating encephalomyelitis (ADEM), and 7 of the 10 (70%) adults with IgM (5) or IgA (5) had optic neuritis at onset. At the last follow-up, the final diagnoses remained as ADEM in 14 (100%) children and optic neuritis in 6 (86%) adults. The outcome was not different between patients with or without additional classes of antibodies. CONCLUSION: Coexisting IgM and IgA antibodies occurs in 19% of children and adult patients with MOG-IgG-associated disease. The presence of these antibodies does not seem to play a relevant clinical role in the disorder.
Authors: Georg Royl; Tsafack Judicael Fokou; Rittika Chunder; Rakad Isa; Thomas F Münte; Klaus-Peter Wandinger; Markus Schwaninger; Oliver Herrmann; José Manuel Valdueza; Jan Brocke; Martin Willkomm; Dietrich Willemsen; Gerd U Auffarth; Swantje Mindorf; Britta Brix; Angel Chamorro; Anna Planas; Xabier Urra Journal: J Neurol Date: 2019-07-29 Impact factor: 4.849
Authors: Markus Reindl; Kathrin Schanda; Mark Woodhall; Fiona Tea; Sudarshini Ramanathan; Jessica Sagen; James P Fryer; John Mills; Bianca Teegen; Swantje Mindorf; Nora Ritter; Ulrike Krummrei; Winfried Stöcker; Juliane Eggert; Eoin P Flanagan; Melanie Ramberger; Harald Hegen; Kevin Rostasy; Thomas Berger; Maria Isabel Leite; Jacqueline Palace; Sarosh R Irani; Russell C Dale; Christian Probst; Monika Probst; Fabienne Brilot; Sean J Pittock; Patrick Waters Journal: Neurol Neuroimmunol Neuroinflamm Date: 2020-02-05
Authors: Fiona Tea; Deepti Pilli; Sudarshini Ramanathan; Joseph A Lopez; Vera Merheb; Fiona X Z Lee; Alicia Zou; Ganesha Liyanage; Chelsea B Bassett; Selina Thomsen; Stephen W Reddel; Michael H Barnett; David A Brown; Russell C Dale; Fabienne Brilot Journal: Front Immunol Date: 2020-02-06 Impact factor: 7.561