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Hence, the restricted pattern of HSV-2 0ΔNLS and 0ΔRING shedding from mouse eyes was not dependent on host lymphocytes (Fig. 7A vs 7B).
This is due in part to the presence of antigen presenting cells in the donor tissues, which directly activate host lymphocytes by the "direct presentation" process [9].
In contrast, Theileria parva promotes uncontrolled proliferation of infected host lymphocytes [ 53].
To avoid potential cross-reaction with host stroma and infiltrating host lymphocytes, immunoblots were probed with non-rodent antibodies.
Our study examined whether colon adenocarcinoma cells release sFasL, and induce apoptosis of host lymphocytes without direct cell cell contact.
Expression of membrane-bound Fas ligand (mFasL) on colon cancer cells serves as a potential mechanism to inhibit host immune function by inducing apoptosis of host lymphocytes.
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Fites et al. (2013) provided the first evidence for this hypothesis, demonstrating Bd inhibition of host lymphocyte proliferation.
Although a dilution factor could explain these findings, we fail to demonstrate a decrease of host lymphocyte alloreactivity on day zero which would be an efficient way to prove the effectiveness of this approach.
It has been suggested [ 45] that the transient double stranded RNA intermediates produced by the accelerated replication of IHNV 24 hours post infection seem to regulate the expression of trout Toll-like Receptor 3 (rtTLR3) in a unpredictable manner, strongly dependent on viral growth and host lymphocyte recirculation cycles.
Both class I and II molecules are involved in displaying peptide antigen to host T lymphocytes in order to activate immune response [4].
For example, a spliced homolog of cellular interleukin 10 (vIL-10, Ov2.5) has been described, which may serve as a growth factor for the host's lymphocytes and which also may act differently, depending on the animal species infected.
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