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We demonstrated ex vivo that breast cancer cell-secreted factors modulate macrophage differentiation toward the M2 phenotype.
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Complement activation modulates macrophage differentiation and engagement of C5a-C5aR axis has been shown to promote M1 polarization and progression to inflammatory injury and fibrosis [ 88].
Vitamin D has been found to promote the induction of monocytic differentiation to macrophages and to modulate macrophage responses, preventing them from releasing proinflam-matory cytokines and chemokines [ 47].
In preliminary experiments we have observed that TLQP-21 can modulate macrophage function.
The use of MSCs prior to differentiation in tissue engineering may therefore serve as a dynamic approach, through continuous cross-talk between MSCs and the inflammatory cells, to modulate macrophage activation and attenuate the FBR to implanted synthetic scaffolds thus improving the long-term tissue engineering outcome.
In addition, upon macrophage differentiation, the mannose glycopolymer exhibited enhanced uptake in M2-polarized macrophages, an anti-inflammatory macrophage phenotype prevalent in injured tissue.
For instance, intermediate spectra of macrophage differentiation states were reported by Finn et al. [23].
However, owing to the complicated roles of Notch in macrophage differentiation and activation, it is valuable to determine the role of Notch signaling in macrophages during renal fibrogenesis.
Whether M2 macrophages predominate in early human plaques is not known, though M-CSF-driven monocyte to macrophage differentiation may promote such skewing (Figure 1).
C/EBPβ is dramatically induced during macrophage differentiation [12], [13].
Macrophage expression of adipokine receptors for both leptin and adiponectin suggests that adipocytes may also modulate macrophage function [6] [7].
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