Tolerance: cell receptors

Shiv A. Prasad shiv at hiv.med.umn.edu
Mon Jul 19 19:01:32 EST 1993


In article <93197.093239FORSDYKE at QUCDN.QueensU.CA> <FORSDYKE at QUCDN.QueensU.CA> writes:
>  Has anyone noticed the subtle reevaluation of quantitative aspects of
>lymphocyte signalling recently?-of some relevence to the hypothesis that
>tolerance is some function of the number of determinant-receptor reactions at
>the cell surface:
>
>  (i) Williams and Beyers. Nature 356, 746-747 state: "It is generally
>thought that TCRs must be crosslinked to activate a T cell, yet how is
[...]

> (ii)Tamura and Nariuchi. J. Immunology 148, 2370-2377 state: "These
>results indicate that monovalent anti-CD3 is more efficient than divalent
>anti-CD3 in induction of IL2 production and that cross-linkage of the
>TCR/CD3 complex is not necessarily required for T cell clone activation."
>

Don, I missed this one.  Was the monovalent anti-CD3 plate-adsorbed or
soluble?  And if it was soluble, how can one be sure that there were no
aggregates?  Admittedly these are simple-minded critiques, and I could look
up the article, but that would be counterproductive to a discussion :-)

Additionally, what is meant by "T cell clone activation?"  This can be anything
from tyrosine phosphorylation of substrates to IL-2 secretion and proliferation.
Recent work from the labs of Paul Allen and Ron Germain argue that there is
a spectrum of consequences of TCR occupancy that depend on the affinity of the
TCR for the ligand.  A monovalent TCR-ligand interaction might transmit *some*
of these signals.

Nevertheless, there does seem to be a reevaluation of receptor signalling.

--
Shiv A. Prasad				shiv at lenti.med.umn.edu
Dept. of Microbiology			pras0005 at student.tc.umn.edu
Univ. of Minnesota



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