Journal Watch (JW)
Has anyone noticed the subtle reevaluation of quantitative aspects of
lymphocyte signalling over the last few months?
(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
this to occur through the TCR:MHCpep interaction? It seems most
improbable that adjacent MHC molecules will display the same peptides,
and to give a cross-linking signal two MHC molecules displaying the same
peptide would have to be tethered together."
(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."
(iii)Ucker, Meyers and Obermiller J. Immunology 149, 1583-1592 state:
"At low stimulatory dose [of antigen], cells do not respond but they
remain viable for extended periods. At higher dose (operationally in the
normal range), cells proliferate in a dose-dependent fashion. Finally,
at still higher dose, proliferation is inhibited and cells rapidly
become non-viable." "In the simplest sense, it is possible to model the
cellular response as a function of the dose or strength of stimulation. One
high dose of stimulus gives proliferation, two give cell death."
Any comments?
Sincerely,
Don Forsdyke (Discussion leader)
