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Based on this observation, we hypothesized that increased p38 and JNK activity may be causally linked to increased T cell activation-induced cell death observed in infected cells.
Costimulation of TCR with CD46 leads to increased T cell proliferation [12], and affects T cell morphology [13] and polarity [14].
Our results also demonstrate that male TH mice with hyperglycemia and obesity underwent reduction of BMD due to increased T cell inflammation.
In fact, an earlier approach in which an Fc-IL-7 fusion protein was delivered via weekly injections led to increased T cell: B cell ratios in the spleens of humanized NOD-scid γc-/ mice[7].
Because a decrease in viraemia (as for example during antiviral therapy) leads to increased T cell responsiveness, and that this is reversible, indicates that tolerance is actively maintained either directly or indirectly by the virus.
We previously demonstrated that patients with osteolytic bone metastases from different solid tumours showed enhanced spontaneous osteoclastogenesis, due to increased T cell release of pro-osteoclastogenic factors, such as TNF-alpha, IL-7 and RANKL [4].
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A proof-of-principle in vivo immunogenicity assay was next performed in order to establish that targeting the PD-L1 receptor during BCG immunisation could lead to increased T-cell function.
Stimulation of these agonist pathways has been reported to lead to increased T-cell activation, proliferation, expansion, survival, memory formation, TH1 development, and induction of interleukin (IL -2 and IL -2immune responses27, 28.
Lastly, although additional tests are needed, the net analysis of macrophage expression of co-stimulatory molecules (e.g., CD80 and CD86) demonstrated that hydrophobic CNFs may ultimately lead to increased T-cell activation than hydrophilic CNFs.
We show here that 5-Azacytidine treatment leads to increased T-cell recognition of tumor cells.
The decrease in T cells is accompanied by increased homeostatic proliferation, which in turn leads to increased T-cell differentiation, activation, and conversion to the memory phenotype.
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