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In diseases like ARDS, iron excess can exacerbate tissue damage by skewing macrophage polarization toward a pro-inflammatory M1 phenotype

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In particular, differently from studies on purified B cells, the mixed cell population of PBMC resemble the in vivo scenario and, upon stimulation with a specific TLR7 agonist (the so-called Imiquimod), could account for cytokine production as well as triggering of CD40 signaling generating an in vitro B cell proliferating milieu unique for either healthy individuals or patients

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