Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 Nov 24;5(12):107.
doi: 10.3390/jcm5120107.

Inebilizumab, a B Cell-Depleting Anti-CD19 Antibody for the Treatment of Autoimmune Neurological Diseases: Insights from Preclinical Studies

Ding Chen  1 , Sandra Gallagher  2 , Nancy L Monson  3 , Ronald Herbst  4 , Yue Wang  5
Affiliations
Review

Inebilizumab, a B Cell-Depleting Anti-CD19 Antibody for the Treatment of Autoimmune Neurological Diseases: Insights from Preclinical Studies

Ding Chen et al. J Clin Med. .

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.

Keywords: B-cell depletion; CD19; autoimmunity; multiple sclerosis; neuromyelitis optica.

PubMed Disclaimer

Conflict of interest statement

D.C. and N.L.M. declare no conflict of interest. S.G., R.H., and Y.W. are employees of MedImmune.

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Steinman L. Immunology of relapse and remission in multiple sclerosis. Annu. Rev. Immunol. 2014;32:257–281. doi: 10.1146/annurev-immunol-032713-120227. - DOI - PubMed
    1. Zatonska M.J., Lyszczarz A.K., Michalak S., Kozubski W. The Immunology of Neuromyelitis Optica-Current Knowledge, Clinical Implications, Controversies and Future Perspectives. Int. J. Mol. Sci. 2016;17:273. doi: 10.3390/ijms17030273. - DOI - PMC - PubMed
    1. Gilhus N.E., Skeie G.O., Romi F., Lazaridis K., Zisimopoulou P., Tzartos S. Myasthenia gravis—Autoantibody characteristics and their implications for therapy, Nature reviews. Neurology. 2016;12:259–268. - PubMed
    1. Dowben J.S., Kowalski P.C., Keltner N.L. Biological Perspectives: Anti-NMDA Receptor Encephalitis. Perspect. Psychiatr. Care. 2015;51:236–240. doi: 10.1111/ppc.12132. - DOI - PubMed
    1. Kruse J.L., Lapid M.I., Lennon V.A., Klein C.J., Toole O.O., Pittock S.J., Strand E.A., Frye M.A., McKeon A. Psychiatric Autoimmunity: N-Methyl-d-Aspartate Receptor IgG and Beyond. Psychosomatics. 2015;56:227–241. doi: 10.1016/j.psym.2015.01.003. - DOI - PubMed