EETosis mediates galectin-10 crystallization. The graphic shows the temporal course of galectin-10 crystallization in tissues. During stimuli-elicited EETosis, loss of regulated intracellular localization of galectin-10 occasionally causes galectin-10 crystallization in the cytoplasm before cell lysis. Galectin-10 is released by plasma membrane disintegration, which may result in extracellular crystallization by increasing local concentrations. Some galectin-10 is also budded from the plasma membrane within enveloped EVs. Thus, FEG, ETs, and galectin-10–containing EV were associated with varied sizes of CLC. Tissue macrophages can also take up galectin-10 and/or small CLC. ET, extracellular trap; EV, extracellular vesicle; FEG, free extracellular granule. See supplemental Figure 8 in the article by Ueki et al that begins on page 2183.

EETosis mediates galectin-10 crystallization. The graphic shows the temporal course of galectin-10 crystallization in tissues. During stimuli-elicited EETosis, loss of regulated intracellular localization of galectin-10 occasionally causes galectin-10 crystallization in the cytoplasm before cell lysis. Galectin-10 is released by plasma membrane disintegration, which may result in extracellular crystallization by increasing local concentrations. Some galectin-10 is also budded from the plasma membrane within enveloped EVs. Thus, FEG, ETs, and galectin-10–containing EV were associated with varied sizes of CLC. Tissue macrophages can also take up galectin-10 and/or small CLC. ET, extracellular trap; EV, extracellular vesicle; FEG, free extracellular granule. See supplemental Figure 8 in the article by Ueki et al that begins on page 2183.

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