Shiv A. Prasad shiv at
Tue Jul 13 17:49:51 EST 1993

In article <CA26DH.6Fy at> woodward at (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
Dept. of Microbiology			pras0005 at
Univ. of Minnesota

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