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. 2021 Jan 5;11:584116. doi: 10.3389/fimmu.2020.584116

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Copyright © 2021 Wright, Lyon, Chapman, Moots and Edwards

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Cytokines in RA SF prime the neutrophil respiratory burst. (A) IPA predicted up-stream cytokine regulators of gene expression in RA SF neutrophils (IFNG, interferon-γ; GCSF, granulocyte colony stimulating factor; TNF, tumor necrosis factor α; IL1B, interleukin 1β; IL6, interleukin 6). (B) Levels of cytokines measured in RA SF from which the neutrophils sequenced by RNA-seq were isolated. (C) ROS production by RA blood and SF neutrophils (with and without cytokine priming) to fMLP. RA SF (25% v/v) also activates ROS production in healthy neutrophils. Stimulation of neutrophils with RA SF containing soluble immune complexes (D) activates ROS production in cytokine primed neutrophils only, whereas RA SF containing insoluble immune complexes (E) activates ROS production in both primed and unprimed neutrophils.