prions and immune response

[Carmen N. Nichols]

On 22 May 1995, JARDINE P wrote 

> Less likely, but far more interesting, is that even though PrP (sc)
> is presumably different, it still is recognized as "self".
> This is were my thoughts get a little fictional. Could the structure
> of PrP (sc) be in fact un-antigenic in the host because the altered
> portion is in fact similar to another host peptide, and if so, could
> the original appearance of the disease state be catalysed by the
> aberant association of this self-peptide with PrP(c).
> Or could in fact the whole self-propagating PrP(sc) model be a
> little off and there is no mis-formation of PrP(c) catalysed by
> PrP(sc).
> Yes, Questions.
> My brain is starting to hurt.
> PJ Jardine
> 
> 
Today, I'm writing.

Sorry, I can't get used to whose writing what these days.  Anyway, cell 
culture models of infection using neuroblastomas have shown quite 
convincingly that PrPsc will convert PrPc to more PrPsc, by a 
post-translational modification, apparently somewhere along the endosomal 
lysosomal pathway.  I would not like to stick my neck out and say nothing 
else is involved e.g. GAGs are implied in playing an important role, but 
without the PrPsc/PrPc interaction there is no further production of 
PrPsc or disease.

Martin Cann