How does it start?

Ken Frauwirth BioKen frauwirt at bacillus.Berkeley.EDU
Fri Aug 8 01:56:28 EST 1997


In article <5s886h$aii at panix.com>, Ian A. York <iayork at panix.com> wrote:

>This is one of the reasons I'm dubious about the "danger" hypothesis.
>Although there are certainly some viruses which lead cells to produce
>'danger' signals, it's not clear to me that all do.  Perhaps more
>significantly, if the 'danger' signals were more important than the
>'non-self' signals, then you'd predict that viruses (in their quest to
>evade teh immune system) would put more emphasis on blocking 'danger'
>signals than on blocking 'non-self' signals.  While some viruses do block
>cytokines (particularly acute viruses, such as many of the pox viruses)
>the classic chronic viruses (herpesviruses, and to some extent
>adenoviruses) have massive armament directed against the MHC class I
>antigen processing pathway--i.e. they target the non-self pathway, rather
>than the danger system.

               [snip]

>To me this suggests that non-self is a more important signal than danger.
>I recognize that it's suggestive rather than definitive, though.

While I tend to agree with you, I don't think that the blockage of MHC is at
all indicative or the relative importances here.  As long as both "danger"
and MHC signals are necessary, it doesn't matter which one you block.  The
importance of "danger" is thought to be in the actual initiation of an immune
response, whereas the MHC Class I establishes the target.  Blocking either 
one would effectively cripple the immune response.

Ken Frauwirth
-- 
Ken Frauwirth (MiSTie #33025)                         _           _
frauwirt at mendel.berkeley.edu                         |_) *    |/ (_ |\ |
http://www.ocf.berkeley.edu/~frauwirt/               |_) | () |\ (_ | \|  
DNRC Title: Chairman of Joint Commission on In-duh-vidual Affairs



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