re immunol. of B7-1 and B7-2
smori at nmsu.edu
Sat Feb 5 22:25:26 EST 1994
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.
: ______________________________________ _________________________________
: [ 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 || ]
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
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??
Program in Molecular Biology
Department of Chemistry Box 3C
NMSU, Las Cruces
smori at nmsu.edu
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