In article <CA26DH.6Fy at ms.uky.edu>, woodward at seqanal.mi.uky.edu (Jerry
Woodward) wrote:
>> I'm new to the bionet.immunology scene. Since there was nothing to read,
> I decided to post a message and to see if there is anyone out there interested.
> Perhaps we need an alternative way of thinking about the immune response.
> We normally think of a response as an activation event to a foreign antigen.
> Perhaps it is better to see it as an absence of a toleragenic signal. In
> other words, tolerance is the default pathway. There is no such thing as a
> "self" or a "non self" antigen. It is simply the manner in which it is
> presented to the immune system. This is probably controled to a large degree
> by a complex interaction of cytokines.
> The TGFbeta knockout mouse is a case in point. If T cell receptor
> repertoire is so important, why did this mouse come down with massive,
> multifocal autoimmunity? This suggests that we all have a very great number
> of self reactive clones, but that self tolerance is maintained by cytokines
> such as TGFbeta.
> I could go on for a while-- Is there any discussion?
The concept of lack of tolerance is well established in the immunology
world.
Self and non-self are human concepts, but there it is useful since it
is relevant in thinking about the role of the thymus. Supressor cells
had gotten to be a dirty name, but the response of a supressor is to
down modulate an immune response. So there are positive responses that
are both activating and deactivating in nature.
By the way, there was a short review in Immunology today a while ago
that modelled the immune response. It used a cute system of a limited
immune system with 256 antigens (taking advantage of 8 bit computer
systems) and produced kinetics similar to a natural immune response.
I look forward when we know enough about cytokines to make a computer
model which will incorporate soluble factors.
Steve Holland
