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Thus, glycan production or distribution is modulated by B. thetaiotaomicron, and this may involve processes important for signaling and mediating the host mucosal response.
Immune cytokines such as the interferons also utilise JAKs, and play an important role in mediating the host response to development of breast cancer (Allione et al, 1994; Camp et al, 1996; Tannenbaum and Hamilton, 2000).
Cell adhesion pathways have been implicated (Herold et al. 2006) in mediating the host inflammatory cell infiltration response to Influenza A virus, and it was suggested they may be key for modulating the severe histopathology observed in acute influenza virus pneumonia.
Ubiquitin and ubiquitin-like modifiers (Ubls) have emerged as central players in mediating the host innate immune response to infection, and their diversity, coordination by specialized enzymatic cascades, and range of linkage topologies all contribute to an incredibly rich regulatory potential.
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However, when implanted, the topology and ligand landscape of the material will determine the host molecules that bind and the type and behavior of cells that mediate the host response.
As already mentioned, TNF-α often mediates the host tissue injury that occurs in exacerbated inflammation, while IL-10 downmodulates Th1 immunity and minimizes inflammatory tissue damage [39], [48], [49].
These proteins transcriptionally regulate human genes that mediate the host response to bacterial invasion such as chemokines and cytokines.
Each of these segments is found to be flanked by murine endogenous retroviral (ERV) elements which have been known to mediate the host recombination [ 29].
They mediate the host response to Gram-positive bacteria and play a fundamental role in pathogen recognition and activation of innate immunity.
In particular, proteins secreted by pathogens (bacterial, protozoan, fungal, viral or helminth) mediate interactions with the host, because these are present or active at the interface between the pathogen and the host cells, and can regulate or mediate the host responses and/or cause disease [ 5, 6].
Pathogen survival in alveolar macrophages is achieved through a diverse range of mechanisms including the inhibition of phagosome maturation and the suppression of key immuno-regulatory pathways that mediate the host immune response to infection [ 12, 13].
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