Ahmet Eken
Mehmet Fatih Yetki̇n
Fatma Zehra Okus
Şerife Erdem
Mustafa Çakir
Yesim Hali̇loğlu
Zehra Busra Azi̇zoğlu
Hamiyet Dönmez Altuntas
Meral Mi̇rza
Halit Canatan

Abstract

Introduction:

Th17 cells are critical mediators of pathology in several autoimmune diseases including multiple sclerosis (MS). The aim of this study was to quantify Th17 cells and-associated cytokines in the peripheral blood of relapsing remitting multiple sclerosis patients (RRMS). We also aimed to compare those levels in fingolimod-treated, and untreated patients.

Material and Methods:

Fifteen fingolimod administered RRMS, 9 untreated-RRMS patients and 6 healthy controls were evaluated. Their peripheral blood mononuclear cells (PBMCs) were isolated and sera separated. IL-17A+, IL-22+ and GM-CSF+ T-cells were quantified via intracellular cytokine staining after stimulation using flouresecein activated cell sorter. Serum cytokine levels from all groups were measured via enzyme-linked immunosorbent assay (ELISA).

Results:

Fingolimod-treated RRMS patients had reduced number of IL-17A+ (p=0.02), IL-22+ (p=0.05), and GM- CSF+ (p=0.003) T cells in their peripheral blood compared to those of untreated RRMS patients. This is consistent with sequestration of lymphocytes in the secondary lymphoid organs after fingolimod use. However, the levels of same cytokines in the serum were statistically not different.

Conclusions:

Fingolimod treatment reduced circulating IL-17A+, IL-22+ or GM-CSF+ T cells in RRMS patients.

Keywords:

Fingolimod, Multiple sclerosis, IL-17A, IL-22, GM-CSF

VOLUME

7

,

ISSUE

2
August 2019

Correspondence

Ahmet Eken

Email

ahmet.eken@gmail.com

Received

Accepted

Published

Suggested Citation

DOI

License

This work is licensed under the Creative Commons Attribution-NonCommercial-Non-Derivatives 4.0 International License (CC BY-NC-ND 4.0). License