Discriminative expression of CD39 and CD73 in Cerebrospinal fluid of patients with Multiple Sclerosis and Neuro-Behçet’s disease

Bahrini, Khadija; Belghith, Mériam; Maghrebi, Olfa; Bekir, Jihène; Kchaou, M.; Jeridi, Cyrine; Amouri, Rim; Hentati, F.; Belal, Samir; Barbouche, Mohamed‐Ridha

doi:10.1016/j.cyto.2020.155054

Cited by 13 publications

(6 citation statements)

References 39 publications

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“…The CSF and PBMCs expressions of cytokines (IFN-γ, IL-1β, TNF-α, IL-17, IL-6, IL-4, and IL-10) and transcription factors (T-bet, GATA-3, RoR-γt, and Foxp3) were assessed. Primers, as previously reported [ 21 , 22 ], were used for real-time PCR. HPLC-purified oligonucleotides primers were bought from CarthaGenomics Advanced Technologies (Tunis, Tunisia).…”

Section: Methodsmentioning

confidence: 99%

Increased T-bet/GATA-3 and ROR-γt /Foxp3 Ratios in Cerebrospinal Fluid as Potential Criteria for Definite Neuro-Behçet’s Disease

Belghith

Maghrebi

Cherif

et al. 2022

JCM

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When the central nervous system (CNS) is the primary affected site in an initial attack of Behçet’s disease (BD), the differential diagnosis is particularly challenging. Some cases remain unclassified or qualified as probable neuro-Behçet’s disease (NBD). Several cytokines are involved in the immunopathogenesis of this disease; however, studies establishing the differential cytokine pattern between probable and definite NBD are scarce. Twenty-eight parenchymal NBD patients, diagnosed according to the International Consensus Recommendation (ICR) criteria and classified into definite (D-NBD; n = 17) and probable (P-NBD; n = 11), were sampled at their first neurological symptoms, and compared with healthy control subjects (n = 20). Oligoclonal bands (OCB) of IgG were detected by isoelectric focusing on agarose, and immunoblotting of matched serum and cerebrospinal fluid (CSF) sample pairs. T cell cytokines (INF-γ, IL-4, IL-17, and IL-10) and transcription factors related to Th1, Th2, Th17, and T regulatory populations (respectively T-bet, GATA-3, ROR-γt, and Foxp3) were studied by quantitative RT-PCR in peripheral blood mononuclear cells (PBMCs) and CSF cells. Inflammatory cytokines such as IL-6, TNF-α, and IL-1β were also analyzed. CSF OCB pattern 2 was present in only 1 out of 28 neuro-Behçet’s patients who belonged to the P-NBD group. Two D-NBD patients had OCB in CSF showing pattern 4. In the D-NBD CSF samples, IL-17 and IL-10 expressions were significantly elevated compared to P-NBD. Moreover, D-NBD patients had increased levels of T-bet/GATA-3 and ROR-γt/Foxp3 ratios compared to P-NBD. Furthermore, a significant increase of CSF IL-6 in D-NBD, compared to P-NBD and the controls, was found. In addition to the increased IL-6 level, the data obtained suggest the existence in D-NBD patients of a significantly disrupted balance between Th17 effector and T regulatory cells, as reflected by the enhanced ROR-γt/Foxp3 ratio. This could be considered as an additional criterion for definite neuro-Behçet’s disease.

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Section: Methodsmentioning

confidence: 99%

Increased T-bet/GATA-3 and ROR-γt /Foxp3 Ratios in Cerebrospinal Fluid as Potential Criteria for Definite Neuro-Behçet’s Disease

Belghith

Maghrebi

Cherif

et al. 2022

JCM

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“…However, the alternative population of HLA-G + nTreg isolated from the CSF of MS patients was able to inhibit the proliferation of T cells in response to a polyclonal stimulation [ 116 ]. Alternatively, CD39 + Treg have been recently characterized in the CSF of RRMS at relapse, and a direct correlation between the levels of CD39 mRNA and the expression of IL-10 in the CSF was established in these patients, indicating that Treg from the CSF can maintain some regulatory activity [ 125 ]. In parallel, IL-10 + Treg have been described within demyelinating lesions, suggesting that Treg might also maintain their suppressor activity within MS tissue and not only in the CSF [ 120 ] ( Figure 2 ).…”

Section: Regulatory Cells In the Brain And Csfmentioning

confidence: 99%

Regulatory Cells in Multiple Sclerosis: From Blood to Brain

et al. 2022

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Multiple sclerosis (MS) is a chronic, autoimmune, and neurodegenerative disease of the central nervous system (CNS) that affects myelin. The etiology of MS is unclear, although a variety of environmental and genetic factors are thought to increase the risk of developing the disease. Historically, T cells were considered to be the orchestrators of MS pathogenesis, but evidence has since accumulated implicating B lymphocytes and innate immune cells in the inflammation, demyelination, and axonal damage associated with MS disease progression. However, more recently the importance of the protective role of immunoregulatory cells in MS has become increasingly evident, such as that of myeloid-derived suppressor cells (MDSCs), regulatory T (Treg) and B (Breg) cells, or CD56bright natural killer cells. In this review, we will focus on how peripheral regulatory cells implicated in innate and adaptive immune responses are involved in the physiopathology of MS. Moreover, we will discuss how these cells are thought to act and contribute to MS histopathology, also addressing their promising role as promoters of successful remyelination within the CNS. Finally, we will analyze how understanding these protective mechanisms may be crucial in the search for potential therapies for MS.

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“…Furthermore, increased levels of CD39 and CD73 were detected in the CSF of RRMS patients, although TNF-a levels were also increased. However, an inverse pattern was reported to occur in the PBMC of the same patients (61). Interestingly, the levels of the adenosine deaminase (ADA) (48) were shown to be decreased in lymphocytes of RRMS patients, which suggests ADO signaling termination may be compromised and that there may be an intracellular accumulation of ADO in these cells, since this enzyme may not be converting ADO into inosine, which has immunomodulatory activity (62).…”

Section: Cd39 Cd73 Regulatory T Cells and Ms Regulationmentioning

confidence: 99%

The adenosinergic signaling in the pathogenesis and treatment of multiple sclerosis

et al. 2022

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Multiple sclerosis (MS) is a highly disabling, progressive neurodegenerative disease with no curative treatment available. Although significant progress has been made in understanding how MS develops, there remain aspects of disease pathogenesis that are yet to be fully elucidated. In this regard, studies have shown that dysfunctional adenosinergic signaling plays a pivotal role, as patients with MS have altered levels adenosine (ADO), adenosine receptors and proteins involved in the generation and termination of ADO signaling, such as CD39 and adenosine deaminase (ADA). We have therefore performed a literature review regarding the involvement of the adenosinergic system in the development of MS and propose mechanisms by which the modulation of this system can support drug development and repurposing.

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Discriminative expression of CD39 and CD73 in Cerebrospinal fluid of patients with Multiple Sclerosis and Neuro-Behçet’s disease

Cited by 13 publications

References 39 publications

Increased T-bet/GATA-3 and ROR-γt /Foxp3 Ratios in Cerebrospinal Fluid as Potential Criteria for Definite Neuro-Behçet’s Disease

Increased T-bet/GATA-3 and ROR-γt /Foxp3 Ratios in Cerebrospinal Fluid as Potential Criteria for Definite Neuro-Behçet’s Disease

Regulatory Cells in Multiple Sclerosis: From Blood to Brain

The adenosinergic signaling in the pathogenesis and treatment of multiple sclerosis

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