scholarly journals Thomas Rivers and the EAE model

2005 ◽  
Vol 202 (1) ◽  
pp. 4-4 ◽  
Author(s):  
Heather L. Van Epps

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.

Author(s):  
Sarah Dhaiban ◽  
Mena Al-Ani ◽  
Noha Mousaad Elemam ◽  
Mahmood H Al-Aawad ◽  
Zeinab Al-Rawi ◽  
...  

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.


2008 ◽  
Vol 14 (4) ◽  
pp. 547-549 ◽  
Author(s):  
D. Galimberti ◽  
C. Fenoglio ◽  
C. Comi ◽  
D. Scalabrini ◽  
M. De Riz ◽  
...  

MDC/CCL22 has been detected in the brain of mice with experimental autoimmune encephalomyelitis. MDC/CCL22 cerebrospinal fluid levels were evaluated in 56 patients with multiple sclerosis (MS) and in 17 controls. No significant differences were found, even when stratifying patients according to the disease subtype. Stratifying by gender, significantly increased MDC/CCL22 levels were observed in female patients when compared with female controls and male patients (109.03 versus 98.54 and 99.37 pg/mL, P = 0.034 and 0.018, respectively). Therefore, MDC/CCL22 is likely to play a role in the development of MS in females only, possibly influencing the intracerebral recruitment of Th2 cells, which produce anti-inflammatory cytokines. Multiple Sclerosis 2008; 14: 547—549. http://msj.sagepub.com


Sci ◽  
2021 ◽  
Vol 3 (1) ◽  
pp. 12
Author(s):  
Sarah Dhaiban ◽  
Mena Al-Ani ◽  
Noha Mousaad Elemam ◽  
Mahmood H. Al-Aawad ◽  
Zeinab Al-Rawi ◽  
...  

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.


2019 ◽  
Vol 6 (1) ◽  
pp. 17-58 ◽  
Author(s):  
Bert A. 't Hart

Abstract. Aging Western societies are facing an increasing prevalence of chronic autoimmune-mediated inflammatory disorders (AIMIDs) for which treatments that are safe and effective are scarce. One of the main reasons for this situation is the lack of animal models, which accurately replicate clinical and pathological aspects of the human diseases. One important AIMID is the neuroinflammatory disease multiple sclerosis (MS), for which the mouse experimental autoimmune encephalomyelitis (EAE) model has been frequently used in preclinical research. Despite some successes, there is a long list of experimental treatments that have failed to reproduce promising effects observed in murine EAE models when they were tested in the clinic. This frustrating situation indicates a wide validity gap between mouse EAE and MS. This monography describes the development of an EAE model in nonhuman primates, which may help to bridge the gap.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mir Hadi Jazayeri ◽  
Khadijeh barzaman ◽  
Reza Nedaeinia ◽  
Tayebe Aghaie ◽  
Morteza Motallebnezhad

Abstract Background Different studies have demonstrated the anti-inflammatory effects of human placental extract both in vivo and in vitro. Considering the chronic inflammatory nature of multiple sclerosis (MS) disease, we examined whether or not the administration of human placental extract is able to attenuate the neurological symptoms detected in experimental autoimmune encephalomyelitis (EAE) model of MS. Methods The injected myelin oligodendrocyte glycoprotein (MOG) induced EAE in mice, and treatment began from day 4 post-injection by intraperitoneal administration of 0.2 mg/kg human placental extract, repeated every other day up to day 31 post-injection. At the end of the treatment, luxol fast blue (LBS) staining and hematoxylin and eosin (H&E) staining were performed to evaluate the demyelination of neurons and inflammatory responses, respectively. Further assessed were the serum concentrations of IL-23 and IL-27. Results The administration of human placental extract was able to significantly reduce the mean clinical score in EAE mice, decrease the pro-inflammatory process and attenuate neural demyelination. Moreover, while the serum concentration of IL-23 was significantly diminished in the EAE mice receiving human placental extract compared to the non-treated EAE group, IL-27 concentration was significantly increased. Conclusions Our findings demonstrated the administration of human placental extract could significantly attenuate the neurological symptoms in the EAE model of MS in part through modulating the serum levels of IL-23 and IL-27 and enhancing neuroprotection and myelin repair.


2018 ◽  
Vol 39 (7) ◽  
pp. 1258-1265 ◽  
Author(s):  
Antoine P Fournier ◽  
Maxime Gauberti ◽  
Aurélien Quenault ◽  
Denis Vivien ◽  
Richard Macrez ◽  
...  

An alteration of parenchymal cerebrospinal fluid circulation (CSF) has been proposed to take part in the pathophysiology of multiple sclerosis. By using an intragate T1-weighted high-resolution MRI of the spinal cord of freely breathing mice injected with a gadolinium chelate in the cisterna magna, we show that a parenchymal CSF circulation exists in the spinal cord, in addition to that originally described in the brain. In experimental autoimmune encephalomyelitis, a model of multiple sclerosis, we show a reduction of parenchymal CSF circulation specifically in the spinal cord but not in the brain.


2018 ◽  
Vol 14 (3) ◽  
pp. 147-149
Author(s):  
Sujata Kar ◽  
Kalipada Kar

Background: Multiple sclerosis (MS) is a dangerous neurodegenerative disorder. Various aspects of  the    disease have been studied in experimental animal model. Migration of immune cells to the central nervous system (CNS) is a predominant feature of MS. CD44 molecule has been reported to be involved in many  important biological processes including contribution in severing inflammation in experimental autoimmune encephalomyelitis (EAE). Matrix metalloprotease-9 (MMP-9) interaction with CD44 has been well known to be involved in cellular adhesion, transmigration and inflammation. In this study, we were interested to examine the role of phagocytic cells expressing MMP-9 in resolving EAE. Materials and Methods: C57BL/6 WT and CD44 KO mice were used as EAE animal model. The level of phagocytic cells expressing MMP-9 in the  secondary lymphoid organs were assessed in EAE induced WT as well as CD44 KO animals. Results: EAE severity was found in CD44 KO group compared to WT. Level of CD11b cells (marker of phagocytic cell) in the peritoneal cells expressing MMP-9 was higher in WT compared to CD44 KO. CD11b stained area found to be greater in WT lymph node compared to CD44 KO. Conclusions: This observation suggests the role of CD44 molecule in modulating the immune scenario which is related to disease severity. This study also opens avenues for the specific inflammatory roles of different immune cells in MS.Keywords: multiple sclerosis; EAE; CD44; MMP-9; CD11b; CNS. 


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