Open Access
Baseline Differences in Minor Lymphocyte Subpopulations may Predict Response to Fingolimod in Relapsing–Remitting Multiple Sclerosis Patients
Author(s) -
TenienteSerra Aina,
Hervás José Vicente,
QuirantSánchez Bibiana,
Mansilla María José,
GrauLópez Laia,
RamoTello Cristina,
MartínezCáceres Eva María
Publication year - 2016
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12548
Subject(s) - fingolimod , multiple sclerosis , relapsing remitting , medicine , baseline (sea) , minor (academic) , lymphocyte , immunology , biology , fishery , political science , law
Summary Aims Fingolimod, oral treatment for relapsing–remitting multiple sclerosis (RRMS), is an agonist of sphingosine and its metabolite S1P that binds their receptors, blocking the egress of lymphocytes from lymph nodes. The aim of this study was immunomonitoring of minor peripheral lymphocyte subpopulations in RRMS patients under treatment with fingolimod and correlation with treatment response. Methods Prospective study. T‐ and B‐cell subpopulations were analyzed using multiparametric flow cytometry in peripheral blood from 14 RRMS patients under treatment with fingolimod at baseline, +1, +3, +6, +9, and +12 months of follow‐up. Response to therapy was assessed at month +12. Results Most changes in minor lymphocyte subpopulations occurred in the first month of treatment and were maintained until the end of follow‐up. The basal percentages of recent thymic emigrants (RTEs) and transitional B cells were lower in responder patients than in nonresponders. After 1 month of follow‐up, the percentages of late effector memory CD4 + T cells in peripheral blood were higher in responder patients. Conclusion If confirmed in a bigger cohort of patients, analysis of percentages of minor lymphocyte subpopulations in peripheral blood of patients with RRMS prior and after +1 month of treatment might predict clinical response to fingolimod.