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Promising shape memory response was obtained from the active VG samples when their surface temperatures were varied from 20 °C to 65°CC.
An enhanced memory response was shown after polysaccharide challenge.
Taken together, these data indicate that a specific memory response was present after tumor cure and argue against a long lasting non-specific increase in non-immune antitumor mechanisms.
As shown in figure 7B (3 versus 6) the IgG anti-NIP titer of the memory response was 5 10 fold lower in the 9B9 treated group (figure 7B group 6) as compared to the 5A12 treated group (figure 7B group 3).
Based on the previously established cut-off values (Figure 4), a significantly higher proportion of memory response was found in the subjects without active disease (5/11, 45.4%) compared with those with active TB (0/11, 0%) (p = 0.03) (Figure 5).
Her in vitro immune response fell dramatically after the end of the formal study, suggesting that a memory response was not being established.
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A memory response is established following primary antigen exposure that stays more or less constant.
The potent memory response is not only directed against the OVA epitope, but also toward a broader range of B16 antigens.
In response to re-encountered antigens, memory B cells robustly secrete antibodies against the pathogen and this memory response is much faster than that of primary B cells due to quantitative and qualitative changes in antigen-specific B cells and helper T cells.
This kind of pathogen-specific memory response is seen after both infections and vaccinations.
Antibody production during both the first and an immunological memory response is disturbed by Zn deficiency [ 9, 10], indicating that Zn is necessary for optimal results following vaccination.
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