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She suggested MF59 might even overstimulate the immune system and create more target cells for the virus to infect.
In this respect, imaging with scV/Tc potentially provides more target cells than ultrasound agents [23],[28] or MRI agents (unpublished data) that, due to their relatively large size, are confined to the intravascular space targeting only VEGFRs on luminal endothelial cells.
This could reflect intrinsic differences between mouse and human NSCs, but might still be attainable by altering some experimental parameters such as infecting more target cells, extending culturing conditions, and incubating target cells with a rho-kinase inhibitor small molecule, shown to enhance survival of human ES cells [30], [31].
This rebound is due to the fact that with less infection, more target cells become available, which increases the chance for virus to infect a cell and, therefore, to rekindle infection.
Thus, suggesting that EBOV-infected macrophages and DC produce inflammatory mediators and chemokines able to recruit additional macrophages and DC to areas of infection, making more target cells available for viral exploitation and further amplifying an already deregulated host response.
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Even though the local production of chemokines attracts more HIV target cells, chemokines may act as competitors for binding CCR5 and CXCR4 receptors [ 145, 146].
Probably, the massive immune activation in the early stage of the disease favors the virus, as it finds more host target cells to exploit for replication.
After SIV challenge, this quiescent tissue environment was actively maintained by a T-regulatory cell response that rapidly expanded to suppress any immune activation and prevent the generation of more activated target cells to support SIV replication (Genescà and Miller, unpublished data) (Fig. 1).
Competition for attachment sites, and multiple simultaneous NK attacks on single targets, would increase as the effector NK cells more radically outnumbered target cells, and hence should be more pronounced at higher E T ratios.
They too reported that a continuous source of external radiation resulted in more effective target cell cytotoxicity and suggested that this may be related to suboptimal proximity between the luciferin and the hypericin.
EhxA exhibits 61% identity to HlyA, but displays a more narrow target cell specificity and binds erythrocytes less efficiently (Bauer & Welch, 1996b; Stanley et al., 1998;), exhibiting virtually no activity against human leukocytes (Bauer & Welch, 1996b).
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