In article <CA26DH.6Fy at ms.uky.edu> woodward at seqanal.mi.uky.edu (Jerry Woodward) writes:
> 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?
>
Clearly we all have a number of self-reactive clones, but I don't think it's
fair to ascribe all tolerance to cytokine effects. Clonal deletion clearly
plays a role in self tolerance in mice :-) Clonal anergy and clonal ignorance
may also be important players. Cytokine effects may be more local, eg the
ACAID phenomenon in the eye. It's difficult to envision cytokines playing
a role in systemic tolerance, or else we'd never gain immunity against
infectious agents.
--
Shiv A. Prasad shiv at lenti.med.umn.edu
Dept. of Microbiology pras0005 at student.tc.umn.edu
Univ. of Minnesota
