ECTRIMS eLearning

Infiltration of CD39 T cells in the CSF of relapsing-remitting multiple sclerosis patients
Author(s): ,
M Belghith
Affiliations:
Immunology, Institut Pasteur
,
K Bahrini
Affiliations:
Pasteur Institut
,
M Kchaou
Affiliations:
Neurology, Charles Nicolle's Hospital, University hospital
,
N Ben Ali
Affiliations:
Neurology, Charles Nicolle's Hospital, University hospital
,
S Blel
Affiliations:
Neurology, Charles Nicolle's Hospital, University hospital
M.R Barbouche
Affiliations:
Immunology, Pasteur Institut, Tunis, Tunisia
ECTRIMS Learn. Belghith M. 09/16/16; 146803; P963
Meriam Belghith
Meriam Belghith
Contributions
Abstract

Abstract: P963

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - Immunology

Introduction/Objective: Multiple sclerosis is a chronic inflammatory disease of the central nervous system (CNS). It has been reported that effectors T cells involved in the pathogenesis of MS are mainly TH1 and TH17 populations. Indeed, they emerged as crucial players in CNS inflammation associated to disease. The purpose of this study is to characterize the phenotype of TCD4 subpopulation present in the cerebrospinal fluid (CSF) and to investigate biomarkers able to discriminate MS patients from patients with other neurological diseases.

Materiel and methods: We quantified the mRNA of INF-γ, IL-17, IL-10, IL-4, Foxp3 and CD39 in the CSF of 25 patients with relapsing remitting multiple sclerosis (RRMS), 20 patients with Neuro-Behçet disease (NBD) and 20 healthy controls. CD39 expression in the CSF was studied simultaneously with Foxp3 intracellular labeling by flow cytometry.

Results: Our findings show an increased level of INF-γ and IL-17 in the CSF of RRMS and NBD patients compared to controls (p< 0.05). Moreover, measurement of anti-inflammatory cytokines, showed a significant increase of IL-10 in the CSF of NBD compared to other groups (p< 0,001). The evaluation of Foxp3 mRNA expression did not show a significant difference between the 3 groups. Thus, we studied another marker called CD39, which is defined as an ecto-enzyme that cleaves ATP to AMP. We demonstrated that CD39 is highly expressed in CSF of RRMS patients (p< 0,001). However, it is absent in the CSF from control group. Moreover, by cytometry the CD39 does not correlate with Foxp3 labeling in the CSF of RRMS patients.

Conclusion: To conclude, we show an increase of pro-inflammatory cytokines in the CSF particularly INF-γ and IL-17. Furthermore, a strong involvement of CD39+ cells seems to play a role in immunodysregulation in the CSF of RRMS patients.

Disclosure: Meriam Belghith: nothing to disclose"

Abstract: P963

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - Immunology

Introduction/Objective: Multiple sclerosis is a chronic inflammatory disease of the central nervous system (CNS). It has been reported that effectors T cells involved in the pathogenesis of MS are mainly TH1 and TH17 populations. Indeed, they emerged as crucial players in CNS inflammation associated to disease. The purpose of this study is to characterize the phenotype of TCD4 subpopulation present in the cerebrospinal fluid (CSF) and to investigate biomarkers able to discriminate MS patients from patients with other neurological diseases.

Materiel and methods: We quantified the mRNA of INF-γ, IL-17, IL-10, IL-4, Foxp3 and CD39 in the CSF of 25 patients with relapsing remitting multiple sclerosis (RRMS), 20 patients with Neuro-Behçet disease (NBD) and 20 healthy controls. CD39 expression in the CSF was studied simultaneously with Foxp3 intracellular labeling by flow cytometry.

Results: Our findings show an increased level of INF-γ and IL-17 in the CSF of RRMS and NBD patients compared to controls (p< 0.05). Moreover, measurement of anti-inflammatory cytokines, showed a significant increase of IL-10 in the CSF of NBD compared to other groups (p< 0,001). The evaluation of Foxp3 mRNA expression did not show a significant difference between the 3 groups. Thus, we studied another marker called CD39, which is defined as an ecto-enzyme that cleaves ATP to AMP. We demonstrated that CD39 is highly expressed in CSF of RRMS patients (p< 0,001). However, it is absent in the CSF from control group. Moreover, by cytometry the CD39 does not correlate with Foxp3 labeling in the CSF of RRMS patients.

Conclusion: To conclude, we show an increase of pro-inflammatory cytokines in the CSF particularly INF-γ and IL-17. Furthermore, a strong involvement of CD39+ cells seems to play a role in immunodysregulation in the CSF of RRMS patients.

Disclosure: Meriam Belghith: nothing to disclose"

By clicking “Accept Terms & all Cookies” or by continuing to browse, you agree to the storing of third-party cookies on your device to enhance your user experience and agree to the user terms and conditions of this learning management system (LMS).

Cookie Settings
Accept Terms & all Cookies