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The main target cell of H5N1 avian influenza viruses (AIVs) in humans is type II alveolar epithelial cells [3], which express the α2,3-linked sialic acid abundantly [4].
In the case of Human Immunodeficiency Virus (HIV), quiescent T lymphocytes, besides macrophages the main target cell population in the human body, are readily infected by the virus, however do not support efficient replication due to multiple early post entry replication blocks [1].
CD4+ T lymphocytes represent the main target cell population of human immunodeficiency virus (HIV).
Once we had identified SMC as the main target cell for the action of E2 in modulating neointimal hyperplasia, we sought to dissect the molecular mechanisms involved.
Translating these results to macrophages, the main target cell of M. tuberculosis, we demonstrate that infection with M. tuberculosis significantly increases Bim expression, and more importantly, downmodulation of Bim levels after transfection with specific siRNA markedly abrogates MT103-induced apoptosis.
Moreover, human keratinocytes, the main target cell population in epidermal photodamage, irradiated at increasing doses (10, 25, 50 and 100 mJ/cm) were investigated for proliferation, colony formation and induction of apoptosis (TUNEL positivity), respectively.
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Although its main target cells are B lymphocytes, EBV can spread to other cell types [2], [3].
We identified that the main target cells for R5 HIV-1 in the decidua are CD14+ cells.
We, therefore, analyzed autophagy in CD4 T cells and macrophages, the two main target cells of HIV-1, during infection with either X4 or R5 strains.
Results obtained have clearly shown that MVA-B infection induces a strong cytotoxic activity by stimulated CD8+ T lymphocytes (69.8% reduction of target cells), thus demonstrating that the combination of MDDC and MVA-B is able to destroy the main target cells where HIV replicates, which could be used as a direct marker of the efficacy of vaccine candidates [76].
Proximal tubular cells were the main target cells of LPA stimulation and Rho kinase signaling was activated in these cells.
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