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Engagement of pattern recognition receptors (PRRs) by pathogen-associated molecular patterns (PAMP) activates Nrf2 in innate immune cells such as monocytes/macrophages (Mø).
Allergen could be recognized by the immune system via three major mechanisms: 1) engagement of pattern recognition receptors, 2) molecular mimicry of TLR signaling complex molecules, and 3) proteolytic activity.
Engagement of pattern recognition receptors by specific pathogen-associated molecular patterns leads to the activation of nuclear factor kappa B, microtubule-associated protein kinase and inflammasomes (in turn activating Casp-1), as well as interferon responses.
FFA and other lipids have been found to regulate the activation state and immune function of macrophages; saturated fatty acids activate classical inflammatory responses in macrophages and other immune cells through engagement of pattern recognition receptors, including Toll-like receptors (TLRs).
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Indeed, in Trex1−/− cells, type 1 IFN activation has been attributed to engagement of pattern-recognition receptors by cytosolic DNA, which may originate from DNA-repair processes or replication of endogenous retroviruses/retroelements.
This form of sterile inflammation is prototypically initiated by engagement of innate pattern recognition receptors, like toll-like receptors [ 68].
The first line of a host's response to various pathogens is triggered by their engagement of cellular pattern recognition receptors (PRRs).
SE engages TLR2, but at high bacterial concentrations can activate primary murine macrophages via a TLR2-independent pathway, indicating engagement of additional pattern recognition pathways, possibly including NLRs and the inflammasome [36], [37], [43].
How the engagement of specific pattern recognition receptors is related to the cytokines that drive CD4 T cell differentiation is an area of active investigation.
Engagement of other pattern-recognition receptors such as nucleotide-binding oligomerization domain-like receptors (NLRs) and subsequent inflammasome assembly leads to caspase-1 activation and, hence, the production of IL-1β and IL-18 to mediate inflammatory response.
Our results indicate that the extracellular polysaccharides produced by G. formosanum stimulate macrophages via the engagement of multiple pattern-recognition receptors including Dectin-1, CR3 and TLR4, resulting in the activation of Syk, JNK, p38, ERK, and NK-κB and the production of TNF-α.
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