Saturday, 9 June 2012

June 9 - Update 11

Further developments on the clinical understanding of GBS & CIDP (and how to stop it occurring).....

Once again I have simplified the information gathered to try and make it easily understood, with apologies to any medical people if I have over simplified parts, but if I put the text in verbatim, then no-one would even read my blog!  I have taken my material from multiple sources (wikipedia, journals,web pages) - I can't reference all sources (as this would also make my blog unfit for purpose of passing the base information on).

I have recently found an article on potential methods of stopping auto-immune diseases and their symptoms.  In order to understand the research further medical terminology needs to be explained (and this is the cut down version):

T-Cells can be sub-divided into different categories, one being Treg - Which are regulatory cells that shut down the immune responses after they have destroyed invading cells (thus causing auto-immune diseases). Normally these cells exist with a ratio of less than 1 to 10 (<1:10) to other T-Cells, the proposed solution increases this ratio to over 1 to 1 (>1:1).  One component in the Treg (IL-5 or IL-5r"alpha") seems to promote activation of relevant antigens (IL-4, CD4, CD25, FOXP3 specific Treg) and these cells would control auto-immune inflammation, by stopping the cells going beyond their initial activities of destroying the invading cells.

Interleukin-5 (IL-5) promotes induction of antigen specific
CD4+CD25+T regulatory cells that suppress autoimmunity

Studies, so far, have been performed in a laboratory in New South Wales - Australia.  The figures below have been copied directly from their research papers (the explanations are in English!):

Note: All animals were given a strain similar to GBS.
        White = no other drug, Grey = Sham/placebo drug, Black = IL-5

Figures A, shows the reduced clinical effect on the rats given IL-5 (first graph) and the reduced effect of weight loss (second graph).  The drugs were administered at 5,000 units/day for 10 days from the onset of GBS (usually day 12) and had an effect within 2 days.

Figure B, shows the difference in the thickness/disruption of the myelin sheaths/demyelination between a control sample and those treated with IL-5 using an electromicrograph.  The differences at day 14 & 21 are significant!

Figure C, shows the reduction in percentage demyelination over 14 & 21 days seen in Figure B.

Figure D, shows the use of an IL-5 blocker (Day 13) on the Grey Triangles sample in the figure, that halted the effects of IL-5 and brought the effects back up to the level of who had not had IL-5 administered.

Further tests were performed to see if the improvements seen in rats can be translated to humans.  The initial trials on our blood samples seem positive.  Clinical trials are hoped to be started in the next couple of years.

This is a completely different way of stopping the disease, by increasing the number of "good cells" that would prohibit the attack rather than directly going against the cells causing the issue.

This treatment could also impact other diseases such as MS. To me the results look very promising.