MDC/CCL22 intrathecal levels in patients with multiple sclerosis

2008 ◽  
Vol 14 (4) ◽  
pp. 547-549 ◽  
Author(s):  
D. Galimberti ◽  
C. Fenoglio ◽  
C. Comi ◽  
D. Scalabrini ◽  
M. De Riz ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Th2 Cells ◽  
Autoimmune Encephalomyelitis ◽  
Disease Subtype ◽  
Male Patients ◽  
Fluid Levels ◽  
The Brain ◽  
Experimental Autoimmune

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

scholarly journals Reduced spinal cord parenchymal cerebrospinal fluid circulation in experimental autoimmune encephalomyelitis

2018 ◽  
Vol 39 (7) ◽  
pp. 1258-1265 ◽  
Author(s):  
Antoine P Fournier ◽  
Maxime Gauberti ◽  
Aurélien Quenault ◽  
Denis Vivien ◽  
Richard Macrez ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Cerebrospinal Fluid ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Fluid Circulation ◽  
Autoimmune Encephalomyelitis ◽  
Cerebrospinal Fluid Circulation ◽  
Csf Circulation ◽  
The Brain ◽  
Experimental Autoimmune

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.

scholarly journals Myelin Basic Protein–specific T Helper 2 (Th2) Cells Cause Experimental Autoimmune Encephalomyelitis in Immunodeficient Hosts Rather than Protect Them from the Disease

1997 ◽  
Vol 186 (2) ◽  
pp. 307-312 ◽  
Author(s):  
Juan J. Lafaille ◽  
Fabienne Van de Keere ◽  
Albert L. Hsu ◽  
Jody L. Baron ◽  
Werner Haas ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Basic Protein ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Autoimmune Encephalomyelitis ◽  
Preclinical Phase ◽  
Deficient Mice ◽  
Th1 And Th2 ◽  
Experimental Autoimmune

Chronic inflammatory autoimmune diseases such as multiple sclerosis, diabetes, and rheumatoid arthritis are caused by CD4+ Th1 cells. Because Th2 cells antagonize Th1 cell functions in several ways, it is believed that immune deviation towards Th2 can prevent or cure autoimmune diseases. Experimental autoimmune encephalomyelitis (EAE) is a demyelinating disease used as a model for multiple sclerosis. Using an adoptive transfer system we assessed the role of Th1 and Th2 cells in EAE. In vitro generated Th1 and Th2 cells from myelin basic protein (MBP)-specific TCR transgenic mice were transferred into normal and immunodeficient mice. Th1 cells caused EAE in all recipients after a brief preclinical phase. Surprisingly, Th2 cells also caused EAE in RAG-1 KO mice and in αβ T cell–deficient mice, albeit after a longer preclinical phase. Normal or γδ T cell–deficient mice were resistant to EAE induced by Th2 cells. The histopathological features of this disease resembled those of an allergic process. In addition, disease induction by Th1 cells was not altered by coadmininstration of Th2 cells in any of the recipients. These findings indicate that MBP-specific Th2 cells have the potential to induce EAE and that the disease induced by previously activated Th1 cells cannot be prevented by normal lymphocytes nor by previously activated Th2 cells.

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.

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