scholarly journals Interferon-β regulates dendritic cell activation and migration in experimental autoimmune encephalomyelitis

Immunology ◽  
2017 ◽  
Vol 152 (3) ◽  
pp. 439-450 ◽  
Author(s):  
Leesa M. Pennell ◽  
Eleanor N. Fish
Keyword(s):  
Dendritic Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Cell Activation ◽  
Interferon Β ◽  
Dendritic Cell Activation ◽  
Autoimmune Encephalomyelitis ◽  
And Migration ◽  
Experimental Autoimmune

scholarly journals Silybin Alleviates Experimental Autoimmune Encephalomyelitis by Suppressing Dendritic Cell Activation and Th17 Cell Differentiation

2021 ◽  
Vol 12 ◽  
Author(s):  
Huan-Li Yang ◽  
Xiao-Wu Shi
Keyword(s):  
Cell Differentiation ◽  
Dendritic Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th17 Cell ◽  
Cell Activation ◽  
Flavonoid Compound ◽  
Dendritic Cell Activation ◽  
Autoimmune Encephalomyelitis ◽  
Th17 Cell Differentiation ◽  
Experimental Autoimmune

Silybin, a peculiar flavonoid compound derived from the fruit and seeds of Silybum marianum, exhibits strong anti-inflammatory activities. In the present study, we found that silybin effectively alleviated experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), via inhibition of dendritic cell (DC) activation and Th17 cell differentiation. Silybin treatment greatly ameliorated the disease severity and significantly declined inflammation and demyelination of the central nervous system (CNS) of EAE mice. Consistent with the disease development, silybin-treated bone marrow-derived DCs (BM-DCs) exhibited reduced costimulatory molecules (e.g., CD80 and CD86) and MHC II expression. These results demonstrated the distinguished bioactivity of silybin for suppressing DC activation, inhibiting pathogenic Th17 inflammatory cell responses, and, eventually, alleviating EAE severity. Taken together, our results show that silybin has high potential for the development of a novel therapeutic agent for the treatment of autoimmune diseases such as MS.

scholarly journals Interleukin-19 Abrogates Experimental Autoimmune Encephalomyelitis by Attenuating Antigen-Presenting Cell Activation

2021 ◽  
Vol 12 ◽  
Author(s):  
Hiroshi Horiuchi ◽  
Bijay Parajuli ◽  
Hiroyasu Komiya ◽  
Yuki Ogawa ◽  
Shijie Jin ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Mhc Class Ii ◽  
Th17 Cell ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Critical Role ◽  
Autoimmune Encephalomyelitis ◽  
Therapeutic Benefits ◽  
Ms Pathogenesis ◽  
Experimental Autoimmune

Interleukin-19 (IL-19) acts as a negative-feedback regulator to limit proinflammatory response of macrophages and microglia in autocrine/paracrine manners in various inflammatory diseases. Multiple sclerosis (MS) is a major neuroinflammatory disease in the central nervous system (CNS), but it remains uncertain how IL-19 contributes to MS pathogenesis. Here, we demonstrate that IL-19 deficiency aggravates experimental autoimmune encephalomyelitis (EAE), a mouse model of MS, by promoting IL-17-producing helper T cell (Th17 cell) infiltration into the CNS. In addition, IL-19-deficient splenic macrophages expressed elevated levels of major histocompatibility complex (MHC) class II, co-stimulatory molecules, and Th17 cell differentiation-associated cytokines such as IL-1β, IL-6, IL-23, TGF-β1, and TNF-α. These observations indicated that IL-19 plays a critical role in suppression of MS pathogenesis by inhibiting macrophage antigen presentation, Th17 cell expansion, and subsequent inflammatory responses. Furthermore, treatment with IL-19 significantly abrogated EAE. Our data suggest that IL-19 could provide significant therapeutic benefits in patients with MS.

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