This Is MS Multiple Sclerosis Community: Knowledge & Support

[topcat72]

Not sure if any of you have heard of Dr Bernard Becher, but I was alerted to an article in a Swiss paper recently concerning a very novel approach to understanding and combating MS. I have managed to find a brief explanation of the therapy:

http://www.wrgfm.com/news/1774

The other articles are in French/German, but I will try and find what I can.

Sounds very promising!

Raj

[gwa]

The article does sound promising, however, I would like to find out who wrote the piece.

One sentence claims that the researchers have identified cells at the origin of this disease.

If this is an accurate statement, the discovery would be all over the news. Since this article is the first I have read with such a "discovery", I am going to wait and see if other scientists agree with the find.

gwa

[CureOrBust]

I would guess that Tovaxin also "discovers the cells responsible", so I am not supprised its so quiet.

[NHE]

From the tidbits of information that are presented, e.g., Becher, Zurich, and Nature Immunology, a PubMed search suggests that this news report likely has something to do with the IL-18 receptor.

Interleukin 18-independent engagement of interleukin 18 receptor-alpha is required for autoimmune inflammation.
Nat Immunol. 2006 Sep;7(9):946-53.

T helper type 1 (T(H)1) lymphocytes are considered to be the main pathogenic cell type responsible for organ-specific autoimmune inflammation. As interleukin 18 (IL-18) is a cofactor with IL-12 in promoting T(H)1 cell development, we examined the function of IL-18 and its receptor, IL-18R, in autoimmune central nervous system inflammation. Similar to IL-12-deficient mice, IL-18-deficient mice were susceptible to experimental autoimmune encephalomyelitis. In contrast, IL-18Ralpha-deficient mice were resistant to experimental autoimmune encephalomyelitis, indicating involvement of an IL-18Ralpha ligand other than IL-18 with encephalitogenic properties. Moreover, engagement of IL-18Ralpha on antigen-presenting cells was required for the generation of pathogenic IL-17-producing T helper cells. Thus, IL-18 and T(H)1 cells are dispensable, whereas IL-18Ralpha and IL-17-producing T helper cells are required, for autoimmune central nervous system inflammation.

NHE