Hi,
I'm a PhD student who is very interested in the field of immunology.
Recently, the cross-priming pathway by which acceptor professional APC
(= dendritic cells; DC) acquire antigen from donor cells to elicit an
antigen-specific CTL respons has been studied in detail by the group of
N. Bhardwaj et al. (Nature 1998; 392: 86-89 & J Exp Med 1998; 188:
1359-1368. This group demonstrated that the cross-priming phenomenon can
be explained by the phagocytosis, processing and presentation of
antigens derived from apoptotic and not necrotic cells on MHC class I
molecules.
Well now, my question is how this theory fits with the "danger" model of
P. Matzinger (Ann Rev Immunol 1994; 12: 991-1045)? According to
Matzinger, the DC must become activated through a danger signal
(necrosis, viral infection,...) in order to function as a professional
(effector) APC capable of activating virgin T cells. As I understood
from this latter model, apoptosis does not represent "danger". Is
something wrong with the way I look at these models or is there a
distinct discrepancy?
Any suggestion?
Viggo VT
