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10.4049/jimmunol.1402164

http://scihub22266oqcxt.onion/10.4049/jimmunol.1402164
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suck abstract from ncbi


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pmid25870242      J+Immunol 2015 ; 194 (10): 4891-900
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  • Ex vivo and in vitro effect of serum amyloid A in the induction of macrophage M2 markers and efferocytosis of apoptotic neutrophils1 #MMPMID25870242
  • Sun L; Zhou H; Zhu Z; Yan Q; Wang L; Liang Q; Ye RD
  • J Immunol 2015[May]; 194 (10): 4891-900 PMID25870242show ga
  • Macrophages affect the magnitude and duration of inflammatory response in a functionally heterogeneous manner. The phenotype of macrophages is maintained through a reversible homeostatic mechanism. A number of determinants that modulate macrophage plasticity have been identified, although the precise mechanisms are not fully understood. Here we report that stimulation of isolated human blood monocytes and mouse bone marrow-derived macrophages with human serum amyloid A (SAA), a major acute-phase protein, leads to induced expression of macrophage M2 markers including IL-10, Ym1, Fizz-1, MRC1, IL-1Rn and CCL17. The same effect was observed with macrophages exposed to SAA in peritoneal cavity. SAA also increases arginase 1 activity and enhances macrophage efferocytosis of apoptotic neutrophils in mouse macrophages. The induction of M2 markers requires MyD88 and the activation of multiple signaling pathways, but is independent of Stat6. SAA induces IRF4 expression and increases its DNA-binding activity. Silencing IRF4 by siRNA abrogates SAA-induced expression of the M2 markers. These results suggest a potential role for SAA to alter macrophage phenotype and modulate macrophage functions through a MyD88-dependent mechanism that involves IRF4-mediated transcription.
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