Interleukin-17 in Chronic Inflammatory Neurological Diseases

Milovanović, Jelena; Arsenijević, Aleksandar; Stojanović, Bojana; Kanjevac, Tatjana; Arsenijević, Dragana; Radosavljević, Gordana; Milovanović, Marija; Arsenijević, Nebojša

doi:10.3389/fimmu.2020.00947

Cited by 133 publications

(111 citation statements)

References 238 publications

(289 reference statements)

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“…Its pathogenesis primarily involves genetic, environmental, and immune components (42). MS is an inflammatory cascade triggered by autoreactive effector T cells and is associated with immune cells such as B cells, macrophages, and natural killer cells (43)(44)(45)(46). It has been found that medullary EVs present in the cerebrospinal fluid are derived from microglia, and microglia will generate and release IL1-β and MHC-II, indicating that EVs secreted by reactive myeloid cells may trigger neuroinflammation and contribute to the rapid spread and presentation of antigens (47).…”

Section: Evs and Autoimmune Diseases Multiple Sclerosismentioning

confidence: 99%

Role of Extracellular Vesicles in Autoimmune Pathogenesis

Song

Zhang

et al. 2020

Front. Immunol.

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Autoimmune diseases are conditions that emerge from abnormal immune responses to natural parts of the body. Extracellular vesicles (EVs) are membranous structures found in almost all types of cells. Because EVs often transport "cargo" between cells, their ability to crosstalk may be an important communication pathway within the body. The pathophysiological role of EVs is increasingly recognized in autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, Sjogren's syndrome, Type 1 diabetes, and autoimmune thyroid disease. EVs are considered as biomarkers of these diseases. This article outlines existing knowledge on the biogenesis of EVs, their role as messegers in cellular communication and the function in T/B cell differentiation and maturation, and focusing on their potential application in autoimmune diseases.

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Section: Evs and Autoimmune Diseases Multiple Sclerosismentioning

confidence: 99%

Role of Extracellular Vesicles in Autoimmune Pathogenesis

Song

Zhang

et al. 2020

Front. Immunol.

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“…However, IL-17 does not stimulate IL-8 expression in these cells, which contradicts early reports that IL-17-induces IL-8 expression in different cell types [17][18][19][20]. Induction of cytokine expression by IL-17 in these leukemia cells could have strong biological relevance in vivo because increases in IL-17 level in a tumor microenvironment can trigger induction of other cytokines including chemokines that could generate combination of proinflammatory, anti-inflammatory and chemotactic responses [16][17][18][19][20]54]; [79][80][81]. IL-2 is a proinflammatory cytokine [118], which also regulates helper T cell differentiation [119].…”

Section: Discussionmentioning

confidence: 55%

“…Similarly, expression of IL-17 R-like protein has been detected in androgen independent prostate cancer cell lines and it has been implicated in conferring resistance to apoptosis and promoting prostate cancer via MM7-induced epithelial-to-mesenchymal transition [75][76][77]. IL-17 is implicated in CNS and other neurological diseases [78][79][80], and psoriasis [81][82][83]. Recent reports suggest potential role for IL-17 in the "cytokine storm event" seen in advance Coronavirus Disease 2019 (COVID-19) infection with inflammation, and pro-thrombic events in severe COVID-19 patients [84][85][86][87].…”

Section: Introductionmentioning

confidence: 99%

IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells

Adunyah¹,

Akomeah²,

Arthur³

et al. 2021

Interleukins - The Immune and Non-Immune Systems’ Related Cytokines

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Human Interlekin-17 is produced by memory activated CD4+ T cells and other cells. It was initially considered unique in that its specific receptor is distinct from other cytokine receptors. IL-17 receptor is ubiquitously expressed by different cells including T cells. IL-17 plays a role in regulating growth, immune response and pro-inflammatory responses. It regulates differentiation of a subset of Th0 cells into Th-17 cells, which produce IL-17-induced cytokines. The IL-17R belongs to type 1 cytokine receptors. IL-17 belongs to a superfamily of its own, which includes IL-17A, IL-17B, IL-17C, IL-17E and IL-17F. These members of IL-17 superfamily have some sequence homology but bind to different receptors. Prior to this investigation, limited information existed on the effects of IL-17A in human leukemia cell lines. Our results show that IL-17A promotes growth, anti-apoptotic effects, chemotaxis, cytokine expression and transcriptional factor activation in leukemia cells. IL-17A activates multiple signaling pathways including PI-3 K, Jak–STAT, Raf-ERK1/2 and SRC kinase pathways, which mediate different biological effects of IL-17A in leukemia cells. Our findings implicate IL-17A in leukemia cell growth and survival, supporting potential leukemia therapy via development of anti-IL-17A drugs. This chapter focuses on IL-17A, herein referred to as IL-17.

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“…Perhaps IL-17A plays a more complex role in the cascade of events that lead to PvST. IL-17A signaling mediates the production of chemokines/cytokines such as IL-8, CCL2, and IL-6 ( Milovanovic et al., 2020 ), which were associated with PvST in our analysis. Considering that the miRNA profile in P. vivax infections remains poorly explored, future studies should clarify whether the miRNAs identified here are mainly involved in the regulation of these key inflammatory mediators or play a critical role in platelet function, or both.…”

Section: Discussionmentioning

confidence: 78%

The Interface Between Inflammatory Mediators and MicroRNAs in Plasmodium vivax Severe Thrombocytopenia

Santos

Coimbra

Sousa

et al. 2021

Front. Cell. Infect. Microbiol.

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Severe thrombocytopenia can be a determinant factor in the morbidity of Plasmodium vivax, the most widespread human malaria parasite. Although immune mechanisms may drive P. vivax-induced severe thrombocytopenia (PvST), the current data on the cytokine landscape in PvST is scarce and often conflicting. Here, we hypothesized that the analysis of the bidirectional circuit of inflammatory mediators and their regulatory miRNAs would lead to a better understanding of the mechanisms underlying PvST. For that, we combined Luminex proteomics, NanoString miRNA quantification, and machine learning to evaluate an extensive array of plasma mediators in uncomplicated P. vivax patients with different degrees of thrombocytopenia. Unsupervised clustering analysis identified a set of PvST-linked inflammatory (CXCL10, CCL4, and IL-18) and regulatory (IL-10, IL-1Ra, HGF) mediators. Among the mediators associated with PvST, IL-6 and IL-8 were critical to discriminate P. vivax subgroups, while CCL2 and IFN-γ from healthy controls. Supervised machine learning spotlighted IL-10 in P. vivax-mediated thrombocytopenia and provided evidence for a potential signaling route involving IL-8 and HGF. Finally, we identified a set of miRNAs capable of modulating these signaling pathways. In conclusion, the results place IL-10 and IL-8/HGF in the center of PvST and propose investigating these signaling pathways across the spectrum of malaria infections.

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Interleukin-17 in Chronic Inflammatory Neurological Diseases

Cited by 133 publications

References 238 publications

Role of Extracellular Vesicles in Autoimmune Pathogenesis

Role of Extracellular Vesicles in Autoimmune Pathogenesis

IL-17 Biological Effects and Signaling Mechanisms in Human Leukemia U937 Cells

The Interface Between Inflammatory Mediators and MicroRNAs in Plasmodium vivax Severe Thrombocytopenia

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