B cell and aquaporin-4 antibody relationships with neuromyelitis optica spectrum disorder activity.


Journal

Annals of clinical and translational neurology
ISSN: 2328-9503
Titre abrégé: Ann Clin Transl Neurol
Pays: United States
ID NLM: 101623278

Informations de publication

Date de publication:
02 Sep 2024
Historique:
revised: 11 07 2024
received: 21 12 2023
accepted: 15 07 2024
medline: 2 9 2024
pubmed: 2 9 2024
entrez: 2 9 2024
Statut: aheadofprint

Résumé

This post hoc analysis of the randomized, placebo-controlled N-MOmentum study (NCT02200770) of inebilizumab in neuromyelitis optica spectrum disorder (NMOSD) evaluated relationships between circulating B-cell subsets and aquaporin-4 immunoglobulin G (AQP4-lgG) titers and attacks. Among participants receiving placebo, CD20

Identifiants

pubmed: 39222408
doi: 10.1002/acn3.52171
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024 The Author(s). Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

Références

Forsthuber TG, Cimbora DM, Ratchford JN, Katz E, Stüve O. B cell‐based therapies in CNS autoimmunity: differentiating CD19 and CD20 as therapeutic targets. Ther Adv Neurol Disord. 2018;11:1756286418761697.
Chihara N, Aranami T, Sato W, et al. Interleukin 6 signaling promotes anti‐aquaporin 4 autoantibody production from plasmablasts in neuromyelitis optica. Proc Natl Acad Sci USA. 2011;108(9):3701‐3706.
Lerch M, Schanda K, Lafon E, et al. More efficient complement activation by anti‐aquaporin‐4 compared with anti‐myelin oligodendrocyte glycoprotein antibodies. Neurol Neuroimmunol Neuroinflamm. 2023;10(1):e200059.
Jitprapaikulsan J, Fryer JP, Majed M, et al. Clinical utility of AQP4‐IgG titers and measures of complement‐mediated cell killing in NMOSD. Neurol Neuroimmunol Neuroinflamm. 2020;7(4):e727.
Kessler RA, Mealy MA, Jimenez‐Arango JA, et al. Anti‐aquaporin‐4 titer is not predictive of disease course in neuromyelitis optica spectrum disorder: a multicenter cohort study. Mult Scler Relat Disord. 2017;17:198‐201.
Jarius S, Aboul‐Enein F, Waters P, et al. Antibody to aquaporin‐4 in the long‐term course of neuromyelitis optica. Brain. 2008;131(Pt 11):3072‐3080.
Wilson R, Makuch M, Kienzler AK, et al. Condition‐dependent generation of aquaporin‐4 antibodies from circulating B cells in neuromyelitis optica. Brain. 2018;141(4):1063‐1074.
Damato V, Theorell J, Al‐Diwani A, et al. Rituximab abrogates aquaporin‐4‐specific germinal center activity in patients with neuromyelitis optica spectrum disorders. Proc Natl Acad Sci USA. 2022;119(24):e2121804119.
UPLIZNA™ (inebilizumab‐cdon). Prescribing Information. Horizon Therapeutics (now Amgen Inc); 2020. Accessed May 24, 2023. https://www.accessdata.fda.gov/drugsatfda_docs/label/2020/761142s000lbl.pdf
Cree BAC, Bennett JL, Kim HJ, et al. Inebilizumab for the treatment of neuromyelitis optica spectrum disorder (N‐MOmentum): a double‐blind, randomised placebo‐controlled phase 2/3 trial. Lancet. 2019;394(10206):1352‐1363.
Rensel M, Zabeti A, Mealy MA, et al. Long‐term efficacy and safety of inebilizumab in neuromyelitis optica spectrum disorder: analysis of aquaporin‐4‐immunoglobulin G‐seropositive participants taking inebilizumab for ≥4 years in the N‐MOmentum trial. Mult Scler. 2022;28(6):925‐932.
Cree BA, Bennett JL, Sheehan M, et al. Placebo‐controlled study in neuromyelitis optica‐ethical and design considerations. Mult Scler. 2016;22(7):862‐872.
Bennett JL, Aktas O, Rees WA, et al. Association between B‐cell depletion and attack risk in neuromyelitis optica spectrum disorder: an exploratory analysis from N‐MOmentum, a double‐blind, randomised, placebo‐controlled, multicentre phase 2/3 trial. EBioMedicine. 2022;86:104321.
Streicher K, Morehouse CA, Groves CJ, et al. The plasma cell signature in autoimmune disease. Arthritis Rheumatol. 2014;66(1):173‐184.
Reindl M. Are aquaporin antibody titers useful outcome measures for neuromyelitis optica spectrum disorders? Neurol Neuroimmunol Neuroinflamm. 2020;7(4):e759.
Chihara N, Aranami T, Oki S, et al. Plasmablasts as migratory IgG‐producing cells in the pathogenesis of neuromyelitis optica. PLoS One. 2013;8(12):e83036.
Mei HE, Frölich D, Giesecke C, et al. Steady‐state generation of mucosal IgA+ plasmablasts is not abrogated by B‐cell depletion therapy with rituximab. Blood. 2010;116(24):5181‐5190.
Fichtner ML, Hoehn KB, Ford EE, et al. Reemergence of pathogenic, autoantibody‐producing B cell clones in myasthenia gravis following B cell depletion therapy. Acta Neuropathol Commun. 2022;10(1):154.
Wallace ZS, Mattoo H, Carruthers M, et al. Plasmablasts as a biomarker for IgG4‐related disease, independent of serum IgG4 concentrations. Ann Rheum Dis. 2015;74(1):190‐195.
Mattoo H, Mahajan VS, Della‐Torre E, et al. De novo oligoclonal expansions of circulating plasmablasts in active and relapsing IgG4‐related disease. J Allergy Clin Immunol. 2014;134(3):679‐687.
Kim HJ, Aktas O, Patterson KR, et al. Inebilizumab reduces neuromyelitis optica spectrum disorder risk independent of FCGR3A polymorphism. Ann Clin Transl Neurol. 2023;10:2413‐2420.
Aktas O, Smith MA, Rees WA, et al. Serum glial fibrillary acidic protein: a neuromyelitis Optica Spectrum disorder biomarker. Ann Neurol. 2021;89(5):895‐910.
Aktas O, Hartung HP, Smith MA, et al. Serum neurofilament light chain levels at attack predict post‐attack disability worsening and are mitigated by inebilizumab: analysis of four potential biomarkers in neuromyelitis optica spectrum disorder. J Neurol Neurosurg Psychiatry. 2023;94(9):757‐768.
Graber DJ, Levy M, Kerr D, Wade WF. Neuromyelitis optica pathogenesis and aquaporin 4. J Neuroinflammation. 2008;5:22. doi:10.1186/1742‐2094‐5‐22

Auteurs

Jeffrey L Bennett (JL)

Departments of Neurology and Ophthalmology, Programs in Neuroscience and Immunology, University of Colorado School of Medicine, Anschutz Medical Campus, Aurora, Colorado, USA.

Sean J Pittock (SJ)

Neurology, Laboratory Medicine and Pathology, Center for Multiple Sclerosis and Autoimmune Neurology, Mayo Clinic, Rochester, Minnesota, USA.

Friedemann Paul (F)

Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin, Berlin, Germany.

Ho Jin Kim (HJ)

Department of Neurology, Research Institute and Hospital of National Cancer Center, Goyang, Republic of Korea.

Sarosh R Irani (SR)

Oxford Autoimmune Neurology Group, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK.
Department of Neurology, Mayo Clinic, Jacksonville, Florida, USA.

Kevin C O'Connor (KC)

Department of Neurology and Immunobiology, Yale School of Medicine, New Haven, Connecticut, USA.

Kristina R Patterson (KR)

Horizon Therapeutics (now Amgen Inc., Thousand Oaks, California, USA), Gaithersburg, Maryland, USA.

Michael A Smith (MA)

Horizon Therapeutics (now Amgen Inc., Thousand Oaks, California, USA), Gaithersburg, Maryland, USA.

Michele Gunsior (M)

Horizon Therapeutics (now Amgen Inc., Thousand Oaks, California, USA), Gaithersburg, Maryland, USA.

Nanette Mittereder (N)

Horizon Therapeutics (now Amgen Inc., Thousand Oaks, California, USA), Gaithersburg, Maryland, USA.

William A Rees (WA)

Horizon Therapeutics (now Amgen Inc., Thousand Oaks, California, USA), Gaithersburg, Maryland, USA.

Daniel Cimbora (D)

Horizon Therapeutics (now Amgen Inc., Thousand Oaks, California, USA), Gaithersburg, Maryland, USA.

Bruce A C Cree (BAC)

UCSF Weill Institute for Neurosciences, Department of Neurology, University of California San Francisco, San Francisco, California, USA.

Classifications MeSH