Enhancement of central nervous system remyelination in immune and non-immune experimental models of demyelination

1997 ◽  
Vol 3 (2) ◽  
pp. 76-79 ◽  
Author(s):  
Baziel GM van Engelen ◽  
Kevin D Pavelko ◽  
Moses Rodriguez

Studies in both humans and experimental animals indicate that there is potential for full remyelination following CNS demyelination, but the factors that control the degree of myelin repair are unknown. In the Theiler's virus model of demyelination CNS remyelination can be promoted either by global immunosuppression or by selective immunoglobulin therapy. In this paper we discuss whether immunoglobulin-mediated remyelination is a characteristic of immune-mediated demyelination, or whether immunoglobulin-mediated remyelination also occurs in the toxic-traumatic model of lysolecithin-induced demyelination. Our data support the hypothesis that even in a non-primary immune model of demyelination, manipulating the immune system can be beneficial in myelin repair.

1997 ◽  
Vol 3 (2) ◽  
pp. 71-75 ◽  
Author(s):  
CF Lucchinetti ◽  
JH Noseworthy ◽  
M. Rodriguez

Studies in both human and experimental models demonstrate that myelin repair occurs in the central nervous system and is a normal physiologic response to myelin injury. However, remyelination in MS is often incomplete and limited. The outcome of an actively demyelinating lesion depends on the balance between factors promoting myelin destruction and myelin repair. Experimental models of CNS demyelination provide an opportunity to investigate the morphologic, cellular and molecular mechanisms involved in remyelination. This review focuses on experiments using the Theiler's virus model of demylination which indicate that manipulation of the immune response has the potential to promote endogenous CNS remyelination and functional recovery in MS.


2019 ◽  
Vol 26 (9) ◽  
pp. 1124-1129 ◽  
Author(s):  
Alicja Kalinowska-Lyszczarz ◽  
Mahboobeh Fereidan-Esfahani ◽  
Yong Guo ◽  
Claudia F Lucchinetti ◽  
W Oliver Tobin

Background: Tumor necrosis factor alpha (TNF-alpha) inhibitors, such as infliximab, are commonly used to treat rheumatoid arthritis (RA) and other immune-mediated disorders. Objective: To determine whether infliximab-associated central nervous system (CNS) demyelination can be differentiated from multiple sclerosis (MS). Methods: We present a case of pathologically proven CNS demyelination in a patient treated with infliximab and describe clinical–radiographic–neuropathological findings. Putative mechanisms of TNF-alpha inhibitor-associated CNS demyelination are described. Results and conclusion: Infliximab treatment is associated with CNS inflammatory demyelinating activity, which is histopathologically indistinguishable from MS.


1997 ◽  
Vol 71 (7) ◽  
pp. 5025-5030 ◽  
Author(s):  
F Bihl ◽  
C Pena-Rossi ◽  
J L Guénet ◽  
M Brahic ◽  
J F Bureau

2003 ◽  
Vol 77 (7) ◽  
pp. 4383-4388 ◽  
Author(s):  
Brian P. Schlitt ◽  
Matthew Felrice ◽  
Mary Lou Jelachich ◽  
Howard L. Lipton

ABSTRACT Theiler's murine encephalomyelitis virus (TMEV) persists in the mouse central nervous system principally in macrophages, and infected macrophages in culture undergo apoptosis. We have detected abundant apoptotic cells in perivascular cuffs and inflammatory, demyelinating lesions of SJL mice chronically infected with TMEV. T cells comprised 74% of apoptotic cells, while 8% were macrophages, 0.6% were astrocytes, and ∼17% remained unidentified. In situ hybridization revealed viral RNA in ∼1% of apoptotic cells.


Sign in / Sign up

Export Citation Format

Share Document