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10.4049/jimmunol.1400732

http://scihub22266oqcxt.onion/10.4049/jimmunol.1400732
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C4185228!4185228!25230753
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suck abstract from ncbi


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pmid25230753      J+Immunol 2014 ; 193 (8): 4043-52
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  • IL-5 triggers a cooperative cytokine network that promotes eosinophil precursor maturation #MMPMID25230753
  • Fulkerson PC; Schollaert KL; Bouffi C; Rothenberg ME
  • J Immunol 2014[Oct]; 193 (8): 4043-52 PMID25230753show ga
  • Eosinophils originate in the bone marrow from an eosinophil lineage?committed, IL-5 receptor alpha (IL-5R?)?positive, hematopoietic progenitor (eosinophil progenitor). Indeed, IL-5 is recognized as a critical regulator of eosinophilia and has effects on eosinophil progenitors, eosinophil precursors and mature eosinophils. However, substantial levels of eosinophils remain after IL-5 neutralization or genetic deletion, suggesting that there are alternative pathways for promoting eosinophilia. Herein, we investigated the contributory role of IL-5 accessory cytokines on the final stages of eosinophil differentiation. IL-5 stimulation of low-density bone marrow cells resulted in expression of a panel of cytokines and cytokine receptors, including several ligand-receptor pairs. Notably, IL-4 and IL-4R? were expressed by eosinophil precursors and mature eosinophils. Signaling through IL-4R? promoted eosinophil maturation when IL-5 was present, but IL-4 stimulation in the absence of IL-5 resulted in impaired eosinophil survival, suggesting that IL-4 cooperates with IL-5 to promote eosinophil differentiation. In contrast, CCL3, an eosinophil precursor?produced chemokine that signals through CCR1, promotes terminal differentiation of CCR1-positive eosinophil precursors in the absence of IL-5, highlighting an autocrine loop capable of sustaining eosinophil differentiation. These findings suggest that brief exposure to IL-5 is sufficient to initiate a cytokine cooperative network that promotes eosinophil differentiation of low-density bone marrow cells independent of further IL-5 stimulation.
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