Inebilizumab, a B cell-depleting anti-CD19 antibody for the treatment of autoimmune neurological diseases: Insights from preclinical studies

Ding Chen, Sandra Gallagher, Nancy L. Monson, Ronald Herbst, Yue Wang

Research output: Contribution to journalReview article

Abstract

Exaggerated or inappropriate responses by B cells are an important feature in many types of autoimmune neurological diseases. The recent success of B-cell depletion in the treatment of multiple sclerosis (MS) has stimulated the development of novel B-cell-targeting therapies with the potential for improved efficacy. CD19 has emerged as a promising target for the depletion of B cells as well as CD19-positive plasmablasts and plasma cells. Inebilizumab (MEDI-551), an anti-CD19 antibody with enhanced antibody-dependent cell-mediated cytotoxicity against B cells, is currently being evaluated in MS and neuromyelitis optica. This review discusses the role of B cells in autoimmune neurological disorders, summarizes the development of inebilizumab, and analyzes the recent results for inebilizumab treatment in an autoimmune encephalitis mouse model. The novel insights obtained from these preclinical studies can potentially guide future investigation of inebilizumab in patients.

Original languageEnglish (US)
JournalJournal of Clinical Medicine
Volume5
Issue number12
DOIs
StatePublished - Jan 1 2016

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Autoimmune Diseases
Anti-Idiotypic Antibodies
B-Lymphocytes
Multiple Sclerosis
Therapeutics
Neuromyelitis Optica
Antibody-Dependent Cell Cytotoxicity
Cell- and Tissue-Based Therapy
Plasma Cells
Nervous System Diseases

Keywords

  • Autoimmunity
  • B-cell depletion
  • CD19
  • Multiple sclerosis
  • Neuromyelitis optica

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Inebilizumab, a B cell-depleting anti-CD19 antibody for the treatment of autoimmune neurological diseases : Insights from preclinical studies. / Chen, Ding; Gallagher, Sandra; Monson, Nancy L.; Herbst, Ronald; Wang, Yue.

In: Journal of Clinical Medicine, Vol. 5, No. 12, 01.01.2016.

Research output: Contribution to journalReview article

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