ArticleFrontiers in immunology2026
Antibody-opsonized extracellular traps modulate macrophage responses and attenuate their T cell-associated inflammatory and costimulatory characteristics.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Macrophages and neutrophils coordinate inflammatory and reparative immunity, and dysregulated interactions between these cells contribute to the pathogenesis of immune-mediated inflammatory diseases. While extracellular traps (ETs), formed by neutrophils and other leukocytes, are enriched in citrullinated histones and exert significant pro-inflammatory effects, it remains unclear how distinct macrophage subsets interpret and resolve ET-derived signals. Here we show that macrophage subsets consistent with pro-inflammatory (GM-CSF + LPS + IFN-γ differentiated) or inflammation-resolving (M-CSF + IL-4 differentiated) characteristics, differentially engage with neutrophil-derived ETs and that antibody binding to ETs reshapes these interactions. ETs induce the release of pro-inflammatory cytokines and chemokines in both macrophage subtypes. While inflammation-resolving macrophages readily phagocytose ETs, pro-inflammatory macrophages exhibit limited uptake. Fc domain-dependent ET phagocytosis by both macrophage subsets is significantly enhanced when ETs are opsonized with an anti-citrullinated histone H2A and H4 monoclonal antibody. Opsonized ETs upregulate macrophage expression of genes encoding negative regulators of Mitogen-Activated Protein Kinase (MAPK) signaling and reduce expression of genes encoding pro-inflammatory receptors. Exposure to antibody-opsonized ETs following macrophage activation with LPS and IFN-γ attenuates the T cell-associated features of pro-inflammatory macrophages with reduced surface expression of CD80 and CD86 and decreased secretion of IL-12 and CXCL9. In inflammation-resolving macrophages antibody-opsonized ETs attenuate MAPK-dependent Toll-like receptor responses and inhibit secretion of CXCL9 and CXCL10 while enhancing IL-10 secretion. Together, these findings describe the pro-inflammatory impact of neutrophil-derived ET exposure on macrophages and delineate a previously unrecognized regulatory axis by which antibodies targeting ET components modulate macrophage responses across distinct subsets to attenuate their T cell-associated inflammatory and costimulatory responses, indicating relevance for therapeutic strategies aimed at modulating ET-driven inflammation.
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