Beneficial effects of fingolimod in MS patients with high serum Sema4A levels

PLoS One. 2018 Mar 8;13(3):e0193986. doi: 10.1371/journal.pone.0193986. eCollection 2018.

Abstract

We previously demonstrated that patients with multiple sclerosis (MS) of high serum Sema4A levels are resistant to IFN-β therapy. To further elucidate the role of serum Sema4A as a biomarker for therapeutic stratification in MS patients, it is important to clarify the efficacy of other disease-modifying drugs (DMD) in those with high serum Sema4A levels. Thus, in this study we investigated whether fingolimod has beneficial effects on MS patients with high Sema4A levels. We retrospectively analyzed annualized relapse rate (ARR) and Expanded Disability Status Scale (EDSS) change in 56 relapsing-remitting multiple sclerosis (RRMS) patients who had been treated with fingolimod, including those who switched from IFN-β therapy. The levels of Sema4A in the sera were measured by sandwich ELISA. The implications of Sema4A on the efficacy of fingolimod were investigated by administering recombinant Sema4A-Fc and fingolimod to mice with experimental autoimmune encephalomyelitis (EAE). Retrospective analysis of MS cohort (17 high Sema4A and 39 low Sema4A) demonstrated the effectiveness of fingolimod in those with high serum Sema4A levels, showing reduction of ARR (from 1.21 to 0.12) and EDSS progression (from 0.50 to 0.04). Consistent with this observation, improvement in the disease severity of EAE mice receiving recombinant Sema4A-Fc was also observed after fingolimod treatment. These data suggest that fingolimod could serve as a candidate DMD for managing the disease activity of MS patients with high Sema4A levels.

Publication types

  • Multicenter Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Antirheumatic Agents / therapeutic use*
  • Biomarkers
  • Disease Progression
  • Drug Evaluation
  • Drug Evaluation, Preclinical
  • Drug Resistance
  • Drug Substitution
  • Encephalomyelitis, Autoimmune, Experimental / blood
  • Encephalomyelitis, Autoimmune, Experimental / drug therapy*
  • Female
  • Fingolimod Hydrochloride / therapeutic use*
  • Humans
  • Immunoglobulin Fc Fragments / genetics
  • Immunoglobulin G / genetics
  • Interferon-beta / therapeutic use
  • Lymphocyte Count
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Middle Aged
  • Multiple Sclerosis, Relapsing-Remitting / blood
  • Multiple Sclerosis, Relapsing-Remitting / drug therapy*
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / toxicity
  • Retrospective Studies
  • Semaphorins / blood*
  • Semaphorins / genetics
  • Semaphorins / toxicity
  • Severity of Illness Index
  • Specific Pathogen-Free Organisms
  • Treatment Outcome

Substances

  • Antirheumatic Agents
  • Biomarkers
  • Immunoglobulin Fc Fragments
  • Immunoglobulin G
  • Recombinant Fusion Proteins
  • SEMA4A protein, human
  • Sema4A protein, mouse
  • Semaphorins
  • Interferon-beta
  • Fingolimod Hydrochloride

Grants and funding

This study is supported in part by a Health and Labour Sciences Research Grant on Rare and Intractable Diseases (Validation of Evidence-based Diagnosis and Guidelines, and Impact on QOL in Patients with Neuroimmunological Diseases) from the Ministry of Health, Labour and Welfare of Japan.