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In addition, memory cells generated from these late transferred CD8 T cells adopt homing properties, characteristic of the CM subset.
They are present in the splenic marginal zone rather than memory cells generated in germinal centers.
Likewise, the amount of inflammation, which in the case of a vaccine can be influenced by the addition of an adjuvant, affects the phenotype and number of the memory cells generated, partly because inflammatory signals are required for the efficient expansion and survival of T cells [ 57].
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Therefore memory T cells generated by priming with anti-CD40 exert stronger effector functions and protective immunity.
In particular, CD28Hi memory T cells generated higher levels of IL-2 in response to CD28-mediated co-stimulation.
The reasons for this difference are unclear but might relate to the fact that PPD-specific IL-2-secreting T cells include cross-reactive memory T cells generated by prior BCG vaccination.
The presence of CD4+ T cells greatly impacts the number and quality of CD8+ "memory" T cells generated during immune responses either directly through cell-contact dependent CD40-CD40L interactions [21] or indirectly through third party populations like dendritic cells (DCs) [22].
The presence of memory T cells generated de novo after exposure to a first allogeneic graft might constitute an important risk for subsequent organ transplantations [ 31, 32].
Our findings lead to the conclusion that recall responses from CD4+ memory T cells generated by previous exposure to seasonal H1N1 viruses and also identifies a highly conserved, novel immunodominant CD4+ T cell epitope that would be a promising target for universal epitope-based influenza vaccines.
In this case, rapid activation of cross-reactive DENV-specific memory T cells generated during primary DENV infection appears to trigger strong production of proinflammatory cytokines such as IFN-γ, TNF-α and Il-6, that can directly damage vascular endothelial cells, further resulting in plasma leakage [ 29, 32].
IFN-γ production is known to promote GvL (Yang et al., 2011), and we show that allogeneic memory T cells generated in vitro produce more IFN-γ than naive T cells, and IFN-γ production is further enhanced when p110δ is inactivated.
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