Lee Wetzler (lwetzler at bu.edu) wrote:
: 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 || ]
: [ Boston City Hospital || phone 617-534-4394 ]
: [ Boston University || ]
: [ School of Medicine || fax 617-534-5280 or 4391 ]
: [ 774 Albany Street || ]
: [ Boston, MA 02118 USA || ]
: [______________________________________||_________________________________]
:Dear immunetters,
The story for B7-1 and B7-2 being from the same gene is hard to accept. There
might be some differential splicing of genes that may be going on.
Something that I read and which makes things even more interesting is that
molecules that alone bind to the T- cell receptor on their own fail to
stimulate the T cells to proliferate, causing anergy. If costimulation is
absent the IL-2 mRNA is rapidly degraded. Only when both stimulatory signals
are present is this process inhibited.Among other things IL-4 production is
inhibited
It has been shown that tumour cells that have been trasfected to express B7
receptors can prime CD8+ T cells to produce IL-2, differentiate and into
tumour lysing CTL's. In regular tumour cells lacking the B7 receptor, there
is no CTL activity. cell 71:? chen et al.
To get back to DC's that Lee asked about. Dendritic cells constitutively
express B7-1, so if we see an increased B7-2 expression on dendritic cells may
indicate that the two truly have different functions.
I am glad about this discussion. We have got a good one going.
Any ideas about my other discussion regarding the HIV co receptor??
Cheers
Shahram mori
Program in Molecular Biology
Department of Chemistry Box 3C
NMSU, Las Cruces
NM
880003
smori at nmsu.edu
