Concept for Relapsing disease orderly epitope spread should be Dead

As an editor I have the capacity to modify Posts 

YOU HAVE BEEN DIRECTED TO THIS PAGE BY SOMEONE WHO THINKS THEY ARE BEING CLEVER...EM 

EpubWegmann et al. Targeting T cells responsive to the priming epitope prevent the relapsing phase of experimental autoimmune encephalomyelitis.  J Neuroimmunol. 2013 Jul 15;260(1-2):74-81.

Upon recovery from the initial episode of experimental autoimmune encephalomyelitis (EAE), virtually all SJL mice develop relapsing/remitting episodes of disease. These relapses may occur due to the reactivation of memory T cells initially stimulated as part of the disease-inducing protocol or naïve T-cell populations stimulated by distinct encephalitogens derived from the inflammatory disease process (epitope spread). We have used encephalitogen-specific non-linear peptide octamers to modify the course of relapsing EAE (rEAE) in SJL mice immunized with an oliogodendrocyte-specific protein peptide (OSP 55-71). Our studies show that the peptide-octamers, which target the T cells stimulated by the priming encephalitogen, but not other candidate encephalitogens, prevent rEAE.




How does an infection lead to autoimmunity...along came the concept of epitope spread whereby damage resulting from viral infection lead to the the development of autoimmunity. This is a nice concept and could explain relapsing disease or how MS could develop and there is no question in my mind that immune reactivity to self targets increase as time goes by...but here is the problem when it is taken to extreme. There are some parts of the science fraternity who believe that relapses are the result of epitope spreading from one epitope to another in an orderly fashion. 

About two minutes of thought should tell you that this is probably a rubbish, concept especially as there are hundreds of lesional events (10 or more per relapse) and the important fact that no-one bar a few labs can replicate this ordered response. This new paper is yet another example how one dubious idea can take many many publications to try and break the idea.  

How  would relapses in T cell receptor transgenic mice occur when they only react to one specificity. Need we say more? 

MD2 will point out that we showed that this concept was on shady ground about 8-10 years ago.

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