Targeting IL-6 receptor in the treatment of neuromyelitis optica spectrum: a review of emerging treatment options

ABSTRACT

Introduction: Recent research has shown that IL-6 receptor (IL-6 R) inhibitors like tocilizumab and satralizumab are effective in reducing the relapse rate in patients with NMOSD.

Areas covered: This review article explores current concepts in NMOSD management and focuses on IL-6 R as a therapeutic target. The authors delve into the biological and immunological role of IL-6 in the pathogenesis of NMOSD. Further, the authors summarize the most recent findings on the use of anti-IL-6 R monoclonal antibodies, tocilizumab and satralizumab, in the treatment of NMOSD.

Expert opinion: A better understanding of the role of cytokines in NMOSD may provide the neurologist with novel therapies for this disease. IL-6 R appears to be a central hub to NMOSD pathogenesis and a relevant therapeutic target.

KEYWORDS:

• Neuromyelitis optica spectrum disorder
• interleukin 6
• tocilizumab
• satralizumab
• emerging therapies

Article highlights

• Novel therapies are required to improve the prognosis of patients with NMOSD. The most promising new agents focus on specific branches of the immune system, which are highly effective in modulating inflammation without compromising immunity.

• Drawing from the lessons learned in rheumatology, anti-IL6 receptor monoclonal antibodies like tocilizumab and satralizumab have shown to be effective in decreasing the relapse rates of patients with NMOSD.

• An open issue for these agents is their long-term impact on the immune system (e.g. neutropenia) and the rate of infections, which may be a threat to this patient population.

Acknowledgments

The authors wish to thank the Guthy Jackson Charitable Foundation for ongoing support of studies in NMOSD.

Declaration of interest

M Rosso and S Saxena received support from Verily Life Sciences and Biogen. received support from Verily Life Sciences and Biogen. T Chitnis received personal compensation for advisory board/consulting for Biogen-Idec, Merck Serono, Novartis, Sanofi, Bayer, Celgene, Alexion and received financial support for research activities from Merck Serono and Novartis Pharmaceuticals. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or conflict with the subject matter or materials discussed in this manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.