Experimental autoimmune encephalomyelitis in the common marmoset Callithrix jacchus

Author(s):  
A. Uccelli ◽  
G. L. Mancardi ◽  
D. Giunti ◽  
H. Brok ◽  
L. Roccatagliata ◽  
...  
2015 ◽  
Vol 26 (4) ◽  
pp. 452-464 ◽  
Author(s):  
Ruth Martha Stassart ◽  
Gunther Helms ◽  
Enrique Garea-Rodríguez ◽  
Stefan Nessler ◽  
Liat Hayardeny ◽  
...  

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.


2006 ◽  
Vol 12 (4) ◽  
pp. 369-374 ◽  
Author(s):  
D Merkler ◽  
B Schmelting ◽  
B Czéh ◽  
E Fuchs ◽  
C Stadelmann ◽  
...  

Pathomorphological studies described pathological heterogeneity in patients with multiple sclerosis (MS). Different effector mechanisms might therefore be responsible for lesion formation in MS. The present report shows that myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) in common marmoset monkeys reflects one specific lesional subtype of MS, namely MS pattern II lesions with antibody/complement-mediated damage. MOG-induced EAE in marmoset monkeys will, therefore, provide an ideal model for therapeutic approaches directed against B-cell/antibody/complement in MS.


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