Contribution of the macrophage migration inhibitory factor superfamily of cytokines in the pathogenesis of preclinical and human multiple sclerosis: In silico and in vivo evidences

Fagone, Paolo; Mazzon, Emanuela; Cavalli, Eugenio; Bramanti, Alessia; Petralia, Maria Cristina; Mangano, Katia; Al‐Abed, Yousef; Bramati, Placido; Nicoletti, Ferdinando

doi:10.1016/j.jneuroim.2018.06.009

Cited by 70 publications

(52 citation statements)

References 58 publications

(83 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We also studied the possible diagnostic and prognostic value of TSPAN32 expression in PBMC of MS patients, on the course of the disease. The use of whole-genome expression databases has been largely exploited [25][26][27][28] for the characterization of pathogenic pathways and to identify therapeutic targets for a variety of disorders, including immunoinflammatory and autoimmune diseases [29][30][31][32][33][34][35][36], cancer [37][38][39], and has allowed dismantling pathogenetic pathways [40][41][42], along with the identification of novel tailored therapeutic targets [43][44][45][46].…”

Section: Discussionmentioning

confidence: 99%

Impaired Expression of Tetraspanin 32 (TSPAN32) in Memory T Cells of Patients with Multiple Sclerosis

et al. 2020

Self Cite

View full text Add to dashboard Cite

Tetraspanins are a conserved family of proteins involved in a number of biological processes. We have previously shown that Tetraspanin-32 (TSPAN32) is significantly downregulated upon activation of T helper cells via anti-CD3/CD28 stimulation. On the other hand, TSPAN32 is marginally modulated in activated Treg cells. A role for TSPAN32 in controlling the development of autoimmune responses is consistent with our observation that encephalitogenic T cells from myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) mice exhibit significantly lower levels of TSPAN32 as compared to naïve T cells. In the present study, by making use of ex vivo and in silico analysis, we aimed to better characterize the pathophysiological and diagnostic/prognostic role of TSPAN32 in T cell immunity and in multiple sclerosis (MS). We first show that TSPAN32 is significantly downregulated in memory T cells as compared to naïve T cells, and that it is further diminished upon ex vivo restimulation. Accordingly, following antigenic stimulation, myelin-specific memory T cells from MS patients showed significantly lower expression of TSPAN32 as compared to memory T cells from healthy donors (HD). The expression levels of TSPAN32 was significantly downregulated in peripheral blood mononuclear cells (PBMCs) from drug-naïve MS patients as compared to HD, irrespective of the disease state. Finally, when comparing patients undergoing early relapses in comparison to patients with longer stable disease, moderate but significantly lower levels of TSPAN32 expression were observed in PBMCs from the former group. Our data suggest a role for TSPAN32 in the immune responses underlying the pathophysiology of MS and represent a proof-of-concept for additional studies aiming at dissecting the eventual contribution of TSPAN32 in other autoimmune diseases and its possible use of TSPAN32 as a diagnostic factor and therapeutic target.

show abstract

Section: Discussionmentioning

confidence: 99%

Impaired Expression of Tetraspanin 32 (TSPAN32) in Memory T Cells of Patients with Multiple Sclerosis

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…pathways and therapeutic targets in several diseases, including cancer and autoimmune, fibrotic, neurodegenerative and infectious diseases (22,23,(54)(55)(56)(57)(58)(59). Presti et al (22) utilized RNA-seq data of 281 and 283 DNA-sequenced glioblastoma multiforme and low-grade glioma patients, respectively, to evaluate the expression levels of migration inhibitory factor (MIF) and related genes in glioma.…”

Section: Discussionmentioning

confidence: 99%

Analysis of circular RNA‑associated competing endogenous RNA network in breast cancer

Wang

Dong

et al. 2020

Oncol Lett

View full text Add to dashboard Cite

As the most common type of cancer in female patients, the morbidity and mortality rates of breast cancer (BC) are high, and its incidence is gradually increasing worldwide. However, the underlying molecular and genetic mechanisms involved in the etiopathogenesis of BC remain unclear. Circular RNAs (circRNAs) are a novel type of non-coding RNAs that have been verified to serve a crucial role in tumorigenesis. However, the majority of functions and mechanisms of circRNAs remain unknown. The present study identified 47 differentially expressed circRNAs in a dataset from Gene Expression Omnibus. Using the cancer-specific circRNA database, the potential microRNA (miRNA) response elements, RNA-binding proteins and open reading frames of the candidate circRNAs were predicted. Combing the predictions of miRNAs and target mRNAs, a competing endogenous RNA network was constructed, which may serve as the theoretical basis for further research. Furthermore, the analyses conducted using Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways indicated that candidate circRNAs may serve a role in transcriptional regulation. Moreover, 20 BC tissue specimens and their paired adjacent normal tissue specimens were used to evaluate the expression levels of the screened circRNAs. Thus, the analyses of the raw microarray data conducted in the present study offer perspectives on the exploration of mechanisms associated with BC tumorigenesis with regard to the circRNA-miRNA-mRNA network.

show abstract

“…Initial studies by ourselves and others have primarily evaluated the role of MIF in the pathogenesis of immunoinflammatory and autoimmune diseases and cancer [7,[21][22][23][24][25][26].…”

Section: Mif In Neurodegenerative Diseasesmentioning

confidence: 99%

“…As discussed above, although the upregulation of MIF levels in PD patients could favor disease progression by increasing neuroinflammation, it might also be considered as a compensatory mechanism of catecholamine detoxification [53]. Additional studies are also needed to better understand whether or not MIF may represent a promising biomarker for PD progression and, eventually, therapeutic response and in particular so since the finding may not be disease-specific as increased serum levels of MIF have also been reported in other neurological disorders, including AD and MS [20,21,23,24].…”

Section: Clinical Studiesmentioning

confidence: 99%

The Dichotomic Role of Macrophage Migration Inhibitory Factor in Neurodegeneration

Basile

Battaglia

Bruno

et al. 2020

IJMS

Self Cite

View full text Add to dashboard Cite

Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine expressed by different cell types and exerting multiple biological functions. It has been shown that MIF may be involved in several disorders, including neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS), Parkinson disease (PD), and Huntington disease (HD), that represent an unmet medical need. Therefore, further studies are needed to identify novel pathogenetic mechanisms that may translate into tailored therapeutic approaches so to improve patients’ survival and quality of life. Here, we reviewed the preclinical and clinical studies investigating the role of MIF in ALS, PD, and HD. The emerging results suggest that MIF might play a dichotomic role in these disorders, exerting a protective action in ALS, a pathogenetic action in HD, and a yet undefined and debated role in PD. The better understanding of the role of MIF in these diseases could allow its use as a novel diagnostic and therapeutic tool for the monitoring and treatment of the patients and for eventual biomarker-driven therapeutic approaches.

show abstract

Contribution of the macrophage migration inhibitory factor superfamily of cytokines in the pathogenesis of preclinical and human multiple sclerosis: In silico and in vivo evidences

Cited by 70 publications

References 58 publications

Impaired Expression of Tetraspanin 32 (TSPAN32) in Memory T Cells of Patients with Multiple Sclerosis

Impaired Expression of Tetraspanin 32 (TSPAN32) in Memory T Cells of Patients with Multiple Sclerosis

Analysis of circular RNA‑associated competing endogenous RNA network in breast cancer

The Dichotomic Role of Macrophage Migration Inhibitory Factor in Neurodegeneration

Contact Info

Product

Resources

About