scholarly journals Uncoupling Protein 2 Has Protective Function during Experimental Autoimmune Encephalomyelitis

2006 ◽  
Vol 168 (5) ◽  
pp. 1570-1575 ◽  
Author(s):  
Susanne Vogler ◽  
Jens Pahnke ◽  
Sophie Rousset ◽  
Daniel Ricquier ◽  
Holger Moch ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Uncoupling Protein ◽  
Uncoupling Protein 2 ◽  
Autoimmune Encephalomyelitis ◽  
Protective Function ◽  
Experimental Autoimmune

scholarly journals Dectin-1 limits central nervous system autoimmunity through a non-canonical pathway

2020 ◽  
Author(s):  
M. Elizabeth Deerhake ◽  
Keiko Danzaki ◽  
Makoto Inoue ◽  
Emre D. Cardakli ◽  
Toshiaki Nonaka ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Myeloid Cells ◽  
Oncostatin M ◽  
List Type ◽  
Autoimmune Encephalomyelitis ◽  
Protective Function ◽  
Lectin Receptor ◽  
Neurologic Disorders ◽  
Cns Autoimmunity ◽  
Experimental Autoimmune

ABSTRACTPathologic roles for innate immunity in neurologic disorders are well-described, but protective aspects of the immune response are less understood. Dectin-1, a C-type lectin receptor (CLR), is largely known to induce inflammation. However, we found that Dectin-1 is protective in experimental autoimmune encephalomyelitis (EAE), while its canonical signaling mediator, Card9, promotes the disease. Notably, Dectin-1 does not respond to heat-killed Mycobacteria, an adjuvant to induce EAE. Myeloid cells mediate the protective function of Dectin-1 in EAE and upregulate gene expression of neuroprotective molecules, including Oncostatin M (Osm) through a non-canonical Card9-independent pathway, mediated by NFAT. Furthermore, we found that the Osm receptor (OsmR) functions specifically in astrocytes to reduce EAE severity. Our study revealed a new mechanism of protective myeloid-astrocyte crosstalk regulated by a non-canonical Dectin-1 pathway and identifies novel therapeutic targets for CNS autoimmunity.Graphical AbstractDectin-1 is a protective C-type lectin receptor (CLR) in experimental autoimmune encephalomyelitis (EAE)Dectin-1 promotes expression of Osm, a neuroprotective IL-6 family cytokine, in myeloid cellsOsmR signaling in astrocytes limits EAE progression and promotes remissionNon-canonical Card9-independent signaling drives a distinct Dectin-1-mediated transcriptional program to induce expression of Osm and other factors with protective or anti-inflammatory functions

scholarly journals Therapeutic Effect of Ginsenoside Rd on Experimental Autoimmune Encephalomyelitis Model Mice: Regulation of Inflammation and Treg/Th17 Cell Balance

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Bo Jin ◽  
Chixiao Zhang ◽  
Yu Geng ◽  
Mei Liu
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Gut Microbiota ◽  
Therapeutic Effect ◽  
Clinical Severity ◽  
Autoimmune Encephalomyelitis ◽  
Protective Function ◽  
Ginsenoside Rd ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is an autoimmune inflammatory disease. Inflammatory infiltrates and demyelination of the CNS are the major characteristics of MS and its related animal model-experimental autoimmune encephalomyelitis (EAE). Immoderate autoimmune responses of Th17 cells and dysfunction of Treg cells critically contribute to the pathogenesis of MS and EAE. Our previous study showed that Ginsenoside Rd effectively ameliorated the clinical severity in EAE mice, but the mechanism remains unclear. In this study, we investigated the therapeutic effect of Ginsenoside Rd on EAE in vivo and in vitro and also explored the potential mechanisms for alleviating the injury of EAE. The results indicated that Ginsenoside Rd was effective for the treatment of EAE in mice and splenocytes. Ginsenoside Rd treatment on EAE mice ameliorated the severity of EAE and attenuated the characteristic signs of disease. Ginsenoside Rd displayed the therapeutic function to EAE by modulating inflammation and autoimmunity, via the downregulation of related proinflammatory cytokines IL-6 and IL-17, upregulation of inhibitory cytokines TGF-β and IL-10, and modulation of Treg/Th17 imbalance. And the Foxp3/RORγt/JAK2/STAT3 signaling was found to be associated with this protective function. In addition, analysis of gut microbiota showed that Ginsenoside Rd also had modulation potential on gut microbiota in EAE mice. Based on this study, we hypothesize that Ginsenoside Rd could be a potential and promising agent for the treatment of MS.

Sign in / Sign up

Export Citation Format

Share Document