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Circulating donor-reactive effector memory T cells have been associated with allograft injury in humans.
However, the majority of memory CD8+ T cells revealed effector memory phenotype expressing CD45RO− CD45RO−D62L−.
TCD8+ cells may be divided into subsets with different phenotypes and functions: naive, central memory, effector memory and effector.
In contrast, CAR T cells with CD28 domains yielded effector memory cells with a genetic signature consistent with enhanced glycolysis.
For clarity we report four previously defined primary memory T cell subsets: T effector memory (Tem), T central memory (Tcm), T double positive effector memory (Tdpem) and T effector memory RA+ (TemRA).
Given the effector and effector memory nature of these CD4−CD8− cells, the effector∶effector memory ratios were examined for both the CD45RA+ and CD45RA− compartments.
Another important finding from our study was that filarial infection was associated with an expanded population of effector memory cells that altered the effector∶effector memory ratio.
However, direct comparison between the effector memory and central memory subsets has not been performed.
Moreover, these CD4+ T cell responses had significant central and effector memory components.
We therefore use the term deregulated effector memory (DEM) cells to describe them.
CD8 T cells can display an "effector", "effector memory", or a "central memory" phenotype [16].
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