scholarly journals IL-11 Induces Encephalitogenic Th17 Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

2019 ◽  
Vol 203 (5) ◽  
pp. 1142-1150 ◽  
Author(s):  
Xin Zhang ◽  
Nazanin Kiapour ◽  
Sahil Kapoor ◽  
Tabish Khan ◽  
Madhan Thamilarasan ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cells ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals The direct deleterious effect of Th17 cells in the nervous system compartment in multiple sclerosis and experimental autoimmune encephalomyelitis: one possible link between neuroinflammation and neurodegeneration

2020 ◽  
Vol 28 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Rodica Balasa ◽  
Smaranda Maier ◽  
Laura Barcutean ◽  
Adina Stoian ◽  
Anca Motataianu
Keyword(s):  
Multiple Sclerosis ◽  
Nervous System ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cells ◽  
Direct Interaction ◽  
Autoimmune Encephalomyelitis ◽  
Cns Inflammation ◽  
Direct Role ◽  
Autoimmune Attack ◽  
Experimental Autoimmune

AbstractThe processes of demyelination and neurodegeneration in the central nervous system (CNS) of multiple sclerosis (MS) patients and experimental autoimmune encephalomyelitis (EAE) are secondary to numerous pathophysiological mechanisms. One of the main cellular players is the Th17 lymphocyte. One of the major functions described for Th17 cells is the upregulation of pro-inflammatory cytokines, such as IL-17 at the level of peripheral and CNS inflammation. This review will focus on the newly described and unexpected, direct role played by the Th17 cells in the CNS of MS patients and EAE models. Th17 and their main cytokine, IL-17, are actively involved in the onset and maintenance of the immune cascade in the CNS compartment as Th17 were found to achieve brain-homing potential. Direct interaction of myelin oligodendrocyte glycoprotein - specific Th17 with the neuronal cells firstly induces demyelination and secondly, extensive axonal damage. The Th17 cells promote an inflammatory B cell response beyond the BBB through the presence of infiltrating Th follicles. Due to their role in preventing remyelination and direct neurotoxic effect, Th17 cells might stand for an important connection between neuroinflammation and neurodegeneration in a devastating disease like MS. The Th17 cell populations have different mechanisms of provoking an autoimmune attack not only in the periphery but also in the CNS of MS patients.

scholarly journals TPL2 mediates autoimmune inflammation through activation of the TAK1 axis of IL-17 signaling

2014 ◽  
Vol 211 (8) ◽  
pp. 1689-1702 ◽  
Author(s):  
Yichuan Xiao ◽  
Jin Jin ◽  
Mikyoung Chang ◽  
Mako Nakaya ◽  
Hongbo Hu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cells ◽  
Autoimmune Encephalomyelitis ◽  
Signaling Mechanism ◽  
Catalytic Activation ◽  
Autoimmune Inflammation ◽  
Receptor Signal ◽  
Inflammatory Action ◽  
Experimental Autoimmune

Development of autoimmune diseases, such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE), involves the inflammatory action of Th1 and Th17 cells, but the underlying signaling mechanism is incompletely understood. We show that the kinase TPL2 is a crucial mediator of EAE and is required for the pathological action of Th17 cells. TPL2 serves as a master kinase mediating the activation of multiple downstream pathways stimulated by the Th17 signature cytokine IL-17. TPL2 acts by linking the IL-17 receptor signal to the activation of TAK1, which involves a dynamic mechanism of TPL2–TAK1 interaction and TPL2-mediated phosphorylation and catalytic activation of TAK1. These results suggest that TPL2 mediates TAK1 axis of IL-17 signaling, thereby promoting autoimmune neuroinflammation.

The action of TH17 cells on blood brain barrier in multiple sclerosis and experimental autoimmune encephalomyelitis

2020 ◽  
Vol 81 (5) ◽  
pp. 237-243 ◽  
Author(s):  
Rodica Balasa ◽  
Laura Barcutean ◽  
Adrian Balasa ◽  
Anca Motataianu ◽  
Corina Roman-Filip ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Blood Brain Barrier ◽  
Th17 Cells ◽  
Brain Barrier ◽  
Autoimmune Encephalomyelitis ◽  
Blood Brain ◽  
Experimental Autoimmune

scholarly journals Lactobacillus acidipiscis Induced Regulatory Gamma Delta T Cells and Attenuated Experimental Autoimmune Encephalomyelitis

2021 ◽  
Vol 12 ◽  
Author(s):  
Saisai Ren ◽  
Xiaorong Zhang ◽  
Hongbing Guan ◽  
Lihong Wu ◽  
Miao Yu ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
Immune System ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cells ◽  
Γδ T Cells ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

Multiple sclerosis is a chronic autoimmune disease involving the central nervous system, and shows a high disability rate. Its pathogenesis is complicated, and there is no good treatment. In recent years, with in-depth studies on the regulation of gastrointestinal flora, the relationship between the mammalian immune system and the intestinal flora has been extensively explored. Changes in the composition and structure of the gastrointestinal flora can affect the characteristics and development of the host immune system and even induce a series of central nervous system inflammation events. The occurrence and development of multiple sclerosis are closely related to the continuous destruction of the intestinal barrier caused by intestinal dysbacteriosis. In this study, we analyzed Lactobacillus acidipiscis in a mouse model of experimental autoimmune encephalomyelitis (EAE). We found that the amount of L. acidipiscis in the intestinal tract was inversely proportional to the progress of EAE development. In addition, the number of CD4+ FOXP3+ regulatory T cells in the mesenteric lymph nodes of mice increased significantly after the mice were fed with L. acidipiscis, and the differentiation of CD4+ T cells to Th1 and Th17 cells was inhibited. However, the protective effect of L. acidipiscis was lost in γδ T cell-deficient mice and hence was concluded to depend on the presence of regulatory γδ T cells in the intestinal epithelium. Moreover, including L. acidipiscis enhanced the development of Vγ1+γδ T cells but suppressed that of Vγ4+γδ T cells. In summary, our results demonstrated the ability of L. acidipiscis to induce generation of regulatory γδ T cells that suppress the development of the encephalomyelitic Th1 and Th17 cells and the progress of EAE.

CCDC134 ameliorated experimental autoimmune encephalomyelitis by suppressing Th1 and Th17 cells

2018 ◽  
Vol 71 ◽  
pp. 158-168 ◽  
Author(s):  
Peng Xia ◽  
Xiaoting Gong ◽  
Lin Xiao ◽  
Yida Wang ◽  
Tianzhuo Zhang ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cells ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune
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