re immunol. of B7-1 and B7-2

Shahram Mori smori at
Sat Feb 5 22:25:26 EST 1994

Lee Wetzler (lwetzler at wrote:
: Paul J Travers (p_travers at 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   ]
: [        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
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??
Shahram mori
Program in Molecular Biology 
Department of Chemistry Box 3C
NMSU, Las Cruces
smori at

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