Thursday, May 22, 2008 3:48:28 PM
from the B cell discovery team, (which happens to be the Bart Haynes team)-
Using assays for plasma levels of soluble Fas ligand, TRAIL and TNFR2, the team has shown evidence of immune cell apoptosis with elevations of microparticles beginning just before plasma viral load ramp-up. They showed that CD4 T cell microparticles can suppress memory B cell activation in vitro. These data raise the hypothesis that one reason for delayed protective antibody responses may be due to apoptotic microparticle-mediated immunosuppression of antibody responses.
the team has shown evidence of immune cell apoptosis with elevations of microparticles beginning just before plasma viral load ramp-up.
CD4 T cell microparticles can suppress memory B cell activation
These data raise the hypothesis that one reason for delayed protective antibody responses may be due to apoptotic microparticle-mediated immunosuppression of antibody responses.
HOW CAN THAT BE DEALT WITH?
HOW CAN YOU INTERFERE WITH (PS-EXPOSING) "MICROPARTICLE-MEDIATED IMMUNOSUPPRESSION" ?
What is CHAVI planning on doing further?
They're planning to see/measure the timing and the extent to which apoptotic cells and the microparticles from those cells suppresses the immune response to HIV.
The team is planning to investigate the effects of inhibition of apoptotic events on the timing of immune responses and control of viremia in SIV-infected macaques.
HOW WILL THEY DO THAT?...............
--------
I'm looking forward to reading about results with Peregrine's mabs.
The work discussed above is in the context of seeing what a successful vaccine will need to do- and how quickly it will need to do what it needs to do, and any promising results using anti-PS in the CHAVI studies to gain insights into vaccine design, have immediate implications and applications for HIV therapeutics.
j
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