Paul J Travers (p_travers at icrf.icnet.uk) wrote:
: Does anyone know anything about the relative binding of B7-1 and B7-2 to
: CD28 vs CTLA-4? Or is the fact that we have two ligands for two receptors,
: one of each pair being induced after activation, mere coincidence?
The affinity of B7-1 (now called CD80) is approximately 20 times higher for
CTLA-4 than for CD28, but ofcourse there is much more CD28 on the T cell
surface. There is currently no info regarding this with B7-2, but people
have told me unofficially that the same holds true.
: On a more pedantic note, does anyone worry that there is already a murine
: cell surface marker B7(2), related (I think) to HSA?
I think this will be solved at the next nomeclature meeting, they just name Cd whatever.
Now I wanted to get back to what Thierry mentioned in his post. I heard A.
Lantovecchia (sp?) talk at Harvard last week and he mentioned the fact that
mature or late dendritic cells are no longer able to process antigen, but are
good at presentation, which might be due to the increased levels of B7-2 on
the mature DC which Thierry mentioned. What do you all think?
Also, there is most likely differential functions of the 2 B7's but we are
just not smart enough to figure it out yet. It is obvious that both ligands
can costimulate, but maybe they like to tickle different types of T cells.
Finally, Thierry mentioned that his group fells that maybe B7-1 and -2 are
from the same gene, which is unlikely given the fact that there is only 26%
homology betwween the two proteins (see the Science article by Freeman, G.J.
on this), but who knows.
Later
______________________________________ _________________________________
[ Lee Wetzler || ]
[ The Maxwell Finland Laboratory || e-mail lwetzler at acs.bu.edu ]
[ for Infectious Diseases || ]
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