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These data lead us to hypothesize a new macrophage phenotype, which we name the switch phenotype.
Of particular interest is the induction of an alternatively activated macrophage phenotype, which promotes tumor development [ 8, 9].
Microglia engaged in phagocytosis generally assume a macrophage phenotype, which is indistinguishable from the macrophage phenotype assumed by monocyte-derived cells.
However, it could be suggested that the blocking of STAT3 and STAT6 might lead to the formation of such a macrophage phenotype which could produce proinflammatory cytokines in response to the anti-inflammatory cytokine IL-13.
The data described above support the hypothesis of the existence of a particular macrophage phenotype, which increases the production of the M2 and decreases the production of the M1 cytokines in the proinflammatory microenvironment.
Moreover we found higher prevalence of M2 macrophage phenotype, which resulted more represented in PCa with ECE (P = 0.0079) and GS 7 to 8 10 and pT3a stage (P = ns).
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After aldosterone treatment, these cells displayed a "classical" activation macrophage phenotype, in which Tnfα, Rantes, Mcp1, and Il12 expression was induced, which was prevented after eplerenone pretreatment, indicating that proinflammatory cytokine expression was through MR [ 25].
The proportions of CD163+ macrophages among CD68+ reflect the proportion of macrophages polarized to M2 phenotype, which was correlated with the histological grade in gliomas [ 28], and these findings were in accordance with our present study.
In addition, iron overload keeps macrophages in an M1 phenotype, which leads to tissue destruction instead of dermal repair.
CSF-1 has been demonstrated as a mediator polarizing macrophages into an M2 phenotype which can promote tumor-induced immunosuppression in established tumors [ 7, 8].
IL-10 inhibits IL-17 and RORγt expression in macrophages and suppresses macrophages toward the proinflammatory M1 phenotype, which is important for the role of IL-10 in mediating the pathogenesis of CIA.
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