I believe Polly is doing, or has done, the experiments to address this
question. I believe she supports the view that apoptotic cells are not
"dangerous". However, as the paper from Bhardwaj et al used virus to induce
apoptosis in monocytes the presentation of exogenous antigen in apoptotic
bodies on MHC class I may depend on the method of inducing apoptosis in the
antigenic cells, as viral infections are certainly "dangerous" according to
Polly's last Nature paper.
Chris
In article <36963186.4075003A at uia.ua.ac.be>,
vigor at uia.ua.ac.be wrote:
> 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
>>
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