Here we show that dendritic cells accumulate the precursor form of the leaderless secretory protein interleukin-18 (pro-interleukin-18) in the cell cytosol and in organelles co-fractionating with endolysosomes. Upon antigen specific contact with T lymphocytes, particulated pro-interleukin-18 decreases rapidly, and the cytokine appears extracellularly, suggesting that exocytosis of pro-interleukin-18-containing organelles is induced. Exocytosis of secretory lysosomes is modulated by calcium: in agreement with this, calcium influx results in secretion of pro-interleukin-18. In turn, pro- interleukin-18 secretion induced by T cells is prevented by the calcium channel blocker nifedipine. Our results demonstrate a novel, calcium-mediated mechanism of post-translational regulation of secretion for interleukin-18, that allows a fast release of the cytokine. (C) 2000 Federation of European Biochemical Societies.
CITATION STYLE
Gardella, S., Andrei, C., Poggi, A., Zocchi, M. R., & Rubartelli, A. (2000). Control of interleukin-18 secretion by dendritic cells: Role of calcium influxes. FEBS Letters, 481(3), 245–248. https://doi.org/10.1016/S0014-5793(00)02015-9
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