Since in our experiments the Tip-DCs turned out to be the most strongly infected cell population and the IFNβ+ Tip-DCs show a higher capacity to produce TNF and iNOS one could speculate that these IFNβ secreting cells are the terminally differentiated most potent cytokine producing innate immune effector cells.
Furthermore, while the rebellion of the Danish filmmakers makes sense within a world dominated by commercial cinema, the rebellion of Blincoe and Thorne is incoherent in a literary world already strongly infected by simplicity, presentism, blankness and a love affair with the cinematic.
In our FACS sorting experiments the IFNβ producing Tip-DCs proved to be the cell population most strongly infected with L. monocytogenes.
Induction of the phytohormone levels is quite similar in WT and the cycam1 mutant, when the %-stimulation by the pathogen is considered, except that the biologically active form of JA, -7- iso-JA-Ile, is induced more strongly in infected WT than cycam1 seedlings.
This is also in agreement with data for CSR1 in C. albicans obtained by infection experiments in mice, where csr1Δ/Δ cells were strongly depleted in infected kidneys (26, 27).
The very early presence of viral DNA in draining lymph nodes strongly suggests that infected cells are one means of viral dissemination from the mucosa.
Finally, B cells, although less numerous, were strongly activated in infected CD150 transgenic mice based on increased CD69 and CD80 expression (Table 1).
Furthermore, NGF expression appeared strongly upregulated in infected bronchial cells with faint GFP staining, suggesting either a paracrine effect or NGF amplification even at low levels of viral replication.
Among the cell lines tested, CagA was strongly phosphorylated in infected AGS, MKN-28, MKN-45, KATO-III, THP-1, J774.A or HT-29 cell lines after 6 hours (Figure 3A, and data not shown), but not in wild-type HEK293 cells, or HEK293 cells stably transfected with expression constructs for human TLR-2 and TLR-5, respectively (Figure 3B D).
Several genes were more strongly expressed in infected macrophages.
Also this concentration increased more strongly for the infected cells.
