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Abstract Details

CD39/CD73 Implication In Neuro-immunological Inflammatory Disorders
Multiple Sclerosis
P2 - Poster Session 2 (5:30 PM-6:30 PM)
15-084
The aim of this work is to determine the expression levels of classical T regulatory markers in the blood and cerebrospinal fluid (CSF) of patients with relapsing-remitting multiple sclerosis (RRMS) and neuro-Behçet disease (NBD) compared to non inflammatory neurological disease (NIND). Our second objective is to investigate the potential role of the subpopulation which expresses the novel regulatory CD39 marker in these patients.

MS and NBD are neuroimmunological inflammatory disorders with many similarities. The real contribution of regulatory cells in these diseases remains controversial. Tregulatory cells (Tregs) characterized as CD4+CD25+FoxP3+ cells have emerged as the key inflammatory diseases suppressing cells. In this context, many studies have found an increased prevalence of circulating CD4+ CD25hi T cells in patients with MS compared to healthy controls. In contrast to RRMS disease, no alteration of the number of T reg cells in the blood of NBD patients was reported . 

We quantified by RT-PCR mRNA expression of different T cell lineage transcription factors and cytokines in cerebrospinal fluid (CSF) and blood from 21 RRMS patients (according to Mc Donald 2010 criteria) and 19 NBD patients (according to International Study Group of BD) and 22 controls (with non inflammatory neurological disorders). All patients were naïve with no disease modifying drugs. Ethical clearance and written consent were obtained for all of them
In the current study, we have shown that there is no difference in the expression of classical regulatory markers: Foxp3, GATA3 and IL-4 in the cerebrospinal fluid of patients with RRMS and NBD disease. However, we noticed a strong CD39 expression in the CSF compartment for the two studied groups of patients compared to controls. In NBD, this CD39 did not correlate with CD73 expression. Furthermore, in the CSF of RRMS, we clearly identified two distinct CD39 populations which co-express or not CD73. CD39+CD73- expression shows a positive correlation with IL17. 

Our results may suggest that CD39+CD73-IL17+ cells could be the inflammatory profile in these neuroimmunological diseases as previously described

Authors/Disclosures

PRESENTER
No disclosure on file
No disclosure on file
No disclosure on file
Samir Belal No disclosure on file
No disclosure on file