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As shown in Figure 5d, p47phox−/− CD8+ memory lymphocytes have more robust PP2A expression than similarly treated WT cells.
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CD8+ memory lymphocytes has a pivotal role in the protective immune response against Lm reinfection.
However, a preferential retention of effector memory over central memory lymphocytes has been observed in most donors.
Memory T lymphocytes have been subdivided into effector/memory (TEM) and central/memory (TCM) subpopulations.
However, this model has been disputed by other investigators [ 7, 8] and CCR7+ naive and memory T lymphocytes have been detected in both normal and inflamed human tissues [ 9].
We conclude that in successfully treated patients autoreactive memory and effector lymphocytes have been eliminated efficiently.
In fact, Mtb-specific lymphocytes have been found to persist as memory cells for an extended period of time after successful chemotherapy [24, 29].
A pool of HIV-1 infected long-lived latently infected memory T-lymphocytes has been reported to be the major reservoir that confers HIV-1 infection resilient to eradication [8], [9], [10].
It has been demonstrated that inhibiting AKT and IKK reduces FOXO3a phosphorylation in CD4+ memory lymphocytes, and that consequently Bim expression was enhanced and apoptosis was induced in the memory lymphocytes.
Compared with memory lymphocytes, ILC2s are activated by cytokines, while memory lymphocytes are activated by specific antigens, thus the memory-like ILC2s are antigen non-specific.
Significant differences were also observed between previously activated memory lymphocytes and naive lymphocytes, indicating a relationship between cell-cycle potential and nanoparticle susceptibility.
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