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These results resemble those found in a mouse model for Listeria monocytogenes infection, in which shortening of the duration of the infectious period did not impact the size of the primary CD8+ T cell response, but diminished the memory population of CD8+ T cells [22].
It has been shown previously that PD-1 expression is enriched within the effector memory population of HIV-1-specific cellsT cells [ 46] and differentially expressed with CD57 [ 48].
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In our own small-scale study of adults, who would have had multiple prior exposures to influenza prior to vaccination resulting in memory populations of influenza-specific T and B cells, we were not able to define a correlate of protection based on responses detected in PBMCs using the IFN-γ ELISpot assay prior to challenge.
This reduction may ultimately diminish the size of the surviving memory population, as the size of the memory pool is closely related to the size of the initial clonal burst [38], [39].
This dominance is maintained in the memory population; the numbers of NP-specific CD8+ T cells exceed all other quantified influenza-specific CD8+ T-cell populations (23 ).
Thus, while we have not yet defined antigen-specific effector and memory populations, because of the lack of methods to mark the filarial-specific cell populations, we have been able to demonstrate alterations in these cell populations ex vivo that likely contribute to the Ag-specific T cell hyporesponsiveness seen previously in vitro [53].
These results suggest that enhanced proliferative response of CD4+ T cells of SLE by TCR stimulation may be caused by increased distribution of the effector memory population and intrinsic defects of SLE CD4+ T cells.
Plasticity of the central memory population is essential for maintenance of specific CD4+ T cells after pathogen clearance, since 90 99 percent of Th1 or Th2 effector cells will undergo apoptosis after antigenic challenge [ 56].
CD4 T cell assistance [ 30, 31] and IL-2 signals during priming have been reported to play some role in the establishment of memory population [ 32].
In the IM immunized group, there was a very low level of proliferation in the CD8+ memory population accompanied by low levels of IFN-γ production in the naïve/effector CD8+ populations, as well as the CD4+ memory population.
Following recall, however, there was a significant impairment of the expansion of the memory population (Fig. 9B).
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