scholarly journals DIAZEPAM EFFECTS ON IMMUNE CELLS ACTIVELY INVOLVED DURING THE DEVELOPMENT OF EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS.

2015 ◽  
Vol 6 ◽  
Author(s):  
Fernández Hurst Nicolás ◽  
Falcón Cristian ◽  
Rupil Lucía ◽  
Cervi Laura ◽  
Monferran Clara ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cells ◽  
Autoimmune Encephalomyelitis ◽  
Experimental Autoimmune

scholarly journals Role of Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

2020 ◽  
Author(s):  
Sarah Dhaiban ◽  
Mena Al-Ani ◽  
Noha Mousaad Elemam ◽  
Mahmood H Al-Aawad ◽  
Zeinab Al-Rawi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cells ◽  
T Regulatory Cells ◽  
Cell Types ◽  
Autoimmune Encephalomyelitis ◽  
The Central Nervous System ◽  
Chronic Autoimmune Disease ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS) characterized by varying degrees of demyelination of uncertain etiology, and is associated with specific environmental and genetic factors. Upon recognition of CNS antigens, the immune cells initiate an inflammatory process which leads to destruction and deterioration of the neurons. Innate immune cells such as macrophages, dendritic cells and natural killer cells are known to play critical roles in the pathogenesis of MS. Also, the activation of peripheral CD4+ T cells by CNS antigens leads to their extravasation into the CNS causing damages that exacerbates the disease. This could be accompanied by dysregulation of T regulatory cells and other cell types functions. Experimental autoimmune encephalomyelitis (EAE) is a mouse model used to study the pathophysiology of MS disease. In this review, we highlight the roles of innate and adaptive immune players in the pathogenesis of MS and EAE.

PGE2/EP4 signaling in peripheral immune cells promotes development of experimental autoimmune encephalomyelitis

2014 ◽  
Vol 87 (4) ◽  
pp. 625-635 ◽  
Author(s):  
Susanne Schiffmann ◽  
Andreas Weigert ◽  
Julia Männich ◽  
Max Eberle ◽  
Kerstin Birod ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cells ◽  
Autoimmune Encephalomyelitis ◽  
Peripheral Immune Cells ◽  
Experimental Autoimmune

scholarly journals Role of Peripheral Immune Cells in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

Sci ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 12
Author(s):  
Sarah Dhaiban ◽  
Mena Al-Ani ◽  
Noha Mousaad Elemam ◽  
Mahmood H. Al-Aawad ◽  
Zeinab Al-Rawi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cells ◽  
Autoimmune Encephalomyelitis ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Exact Etiology ◽  
The Central Nervous System ◽  
Peripheral Immune Cells ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the myelination of the neurons present in the central nervous system (CNS). The exact etiology of MS development is unclear, but various environmental and genetic factors might play a role in initiating the disease. Experimental autoimmune encephalomyelitis (EAE) is a mouse model that is used to study the pathophysiology of MS disease as well as the effects of possible therapeutic agents. In addition, autoreactive immune cells trigger an inflammatory process upon the recognition of CNS antigens, which leads to destruction of the neurons. These include innate immune cells such as macrophages, dendritic cells, and natural killer cells. Additionally, the activation and extravasation of adaptive immune cells such as CD4+ T cells into the CNS may lead to further exacerbation of the disease. However, many studies revealed that immune cells could have either a protective or pathological role in MS. In this review, we highlight the roles of innate and adaptive immune cellular and soluble players that contribute to the pathogenesis of MS and EAE, which may be used as potential targets for therapy.

scholarly journals Choroid Plexus-Selective Inactivation of Adenosine A2A Receptors Protects Against T Cell Infiltration And Experimental Autoimmune Encephalomyelitis

2021 ◽  
Author(s):  
Wu Zheng ◽  
Yijia Feng ◽  
Zhenhai Zeng ◽  
Mengqian Ye ◽  
Huiping Shang ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cells ◽  
Immune Cell ◽  
Cell Infiltration ◽  
Cell Trafficking ◽  
Autoimmune Encephalomyelitis ◽  
Post Immunization ◽  
T Cell Infiltration ◽  
Experimental Autoimmune

Abstract Background: Multiple sclerosis (MS) is one of the most common autoimmune disorders characterized by the infiltration of immune cells into the brain and demyelination. The unwanted immunosuppressive side effect of therapeutically successful natalizumab led us to focus on choroid plexus (CP), a key site for the first wave of immune cell infiltration in experimental autoimmune encephalomyelitis (EAE), for the control of immune cells trafficking. Adenosine A2A receptor (A2AR) is emerging as a potential pharmacological target to control EAE pathogenesis; however, the cellular basis for the A2AR-mediated protection remains undetermined. Methods: In EAE model, we assessed A2AR expression and leukocyte trafficking determinants in CP by immunohistochemistry and qPCR analyses. We determined the effect of the A2AR antagonist KW6002 treatment at days 8-12 or 8-14 post-immunization on T cell infiltration across CP and EAE pathology. We determined the critical role of the CP-A2AR on T cell infiltration and EAE pathology by focal knockdown the CP-A2AR with intracerebroventricular injection of CRE-TAT recombinase into the A2ARflox/flox mice. In cultured CP epithelium, we also evaluated the effect of overexpression of A2ARs or the A2AR agonist CGS21680 treatment on CP permeability and lymphocytes migration. Results: We found the specific upregulation of A2AR in CP in association with enhanced CP gateway activity peaked at day 12 post-immunization in EAE mice. Furthermore, the KW6002 treatment at days 8-12 or 8-14 post-immunization reduced T-cell trafficking across CP and attenuated EAE pathology. Importantly, focal CP-A2AR knockdown attenuated pathogenic infiltration of Th17+ cells across CP via inhibiting CCR6-CCL20 axis through NFκB / STAT3 pathway and protected against EAE pathology. Lastly, activation of A2AR in cultured epithelium by A2AR overexpression or CGS21680 treatment increased the permeability of CP epithelium and facilitated lymphocytes migration. Conclusion: These findings define the CP niche as one of the primary sites of A2AR action whereby A2AR antagonists confer protection against EAE pathology. Thus, pharmacological targeting of the CP-A2AR represents a novel therapeutic strategy for MS by controlling immune cell trafficking across CP.

scholarly journals Thomas Rivers and the EAE model

2005 ◽  
Vol 202 (1) ◽  
pp. 4-4 ◽  
Author(s):  
Heather L. Van Epps
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cells ◽  
Autoimmune Encephalomyelitis ◽  
Eae Model ◽  
The Brain ◽  
Experimental Autoimmune

In the early 1930s, Thomas Rivers and colleagues provided the first evidence that immune cells can attack the brain. Their simple experiments established what is now the most well-studied model of autoimmunity—the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis.

scholarly journals Gasdermin D in peripheral myeloid cells drives neuroinflammation in experimental autoimmune encephalomyelitis

2019 ◽  
Vol 216 (11) ◽  
pp. 2562-2581 ◽  
Author(s):  
Sheng Li ◽  
Yuqing Wu ◽  
Dongxue Yang ◽  
Chunyan Wu ◽  
Chunmei Ma ◽  
...  
Keyword(s):  
T Cell ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Immune Cells ◽  
Nlrp3 Inflammasome ◽  
Myeloid Cells ◽  
Autoimmune Encephalomyelitis ◽  
T Cell Infiltration ◽  
Secondary Lymphoid Organs ◽  
Experimental Autoimmune

The NLRP3 inflammasome is critical for EAE pathogenesis; however, the role of gasdermin D (GSDMD), a newly identified pyroptosis executioner downstream of NLRP3 inflammasome, in EAE has not been well defined. Here, we observed that the levels of GSDMD protein were greatly enhanced in the CNS of EAE mice, especially near the areas surrounding blood vessels. GSDMD was required for the pathogenesis of EAE, and GSDMD deficiency in peripheral myeloid cells impaired the infiltration of immune cells into the CNS, leading to the suppression of neuroinflammation and demyelination. Furthermore, the loss of GSDMD reduced the activation and differentiation of T cell in the secondary lymphoid organs and prevented T cell infiltration into CNS of EAE. The administration of inflammasome-related cytokines partially rescued the impairment of pathogenesis of EAE in GSDMD KO mice. Collectively, these findings provide the first demonstration of GSDMD in peripheral myeloid cells driving neuroinflammation during EAE pathogenesis.

Sign in / Sign up

Export Citation Format

Share Document