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1Finally, we demonstrate that tumor EVs activate macrophages and promote metastatic outgrowth.
2To this end, we present the synthesis of the first AfBPP-TDM probe and report on its ability to activate macrophages.
3Moreover, we have shown the ability of NBL to activate macrophages from the lung parenchyma by the classical and alternative pathways.
4Evidence suggests that activated macrophages contribute to the pathologic response to NM.
5Uptake of R8-NRs by activated macrophages was monitored by two-photon luminescence imaging.
6Results: Activated macrophages efficiently uptake R8-NRs both in vitro and in live animals.
7Background: Activated macrophages contribute to the pathogenesis of inflammatory diseases such as atherosclerosis.
8Conclusions: These data verified that VICM is released by activated macrophages.
9In addition, IRF4-deficient mice showed defective development of alternatively activated macrophages.
10Activated macrophages show increased expression of vimentin, an intermediate filament protein.
11In comparison with untreated macrophages, significant increases in amperometric responses were observed for activated macrophages.
12Immunologically activated macrophages are known to release a cocktail of reactive oxygen and nitrogen species.
13Concomitantly, activated macrophages infiltrated the areas of apoptosis remarkably.
14Reprogramming of intracellular metabolisms is required for the proper polarization and functions of activated macrophages.
15Activated macrophages in turn promote stromal vascularization and angiogenesis even before the formation of cancer.
16Under these conditions, rH-IL2 alone activated macrophages to a tumoricidal state in a concentration dependent fashion.
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