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Blood, 1 May 2007, Vol. 109, No. 9, pp. 3856-3864. Prepublished online as a Blood First Edition Paper on December 27, 2006; DOI 10.1182/blood-2005-06-031377. This Article Full Text (PDF) Supplemental Video All Versions of this Article: blood-2005-06-031377v1 109/9/3856    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Pizzirani, C. Articles by Di Virgilio, F. Search for Related Content PubMed PubMed Citation Articles by Pizzirani, C. Articles by Di Virgilio, F. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 29, 2005 Accepted December 14, 2006 Stimulation of P2 receptors causes release of IL-1-loaded microvesicles from human dendritic cells Cinzia Pizzirani, Davide Ferrari, Paola Chiozzi, Elena Adinolfi, Dorianna Sandona, Erika Savaglio, and Francesco Di Virgilio* Department of Experimental and Diagnostic Medicine, Section of General Pathology, and ICSI, University of Ferrara, Ferrara, Italy Department of Biomedical Sciences, University of Padova, Padova, Italy * Corresponding author; email: fdv{at}unife.it. Dendritic cells (DCs) are professional antigen presenting cells that initiate the immune response by activating T lymphocytes. DCs express plasma membrane receptors for extracellular nucleotides named P2 receptors (P2R). Stimulation of P2R in these cells is known to cause chemotaxis, cytokine release, cell death, and to modulate LPS-dependent differentiation. Here we show that stimulation of the P2X7 receptor subtype (P2X7R) causes fast microvesicle shedding from DC plasma membrane. Vesicle release occurs from both immature and mature DCs, however only vesicles from mature DCs, due to their previous exposure to LPS, contain IL-1. Microvesicles, whether from immature or mature DCs, also contain caspase-1 and -3 and cathepsin D. They also express the P2X7R in addition to other P2R, and known markers of immune cells such as MHC II and CD39. Activation of the P2X7R by extracellular ATP causes IL-1 release from the vesicle lumen. Previous studies demonstrated that high extracellular K+ inhibits IL-1processing and release, here we show that high ionic strength reduces microvesicle shedding when compared to a low ionic strength medium, but strongly increases microvesicle IL-1loading. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: P. Pelegrin, C. Barroso-Gutierrez, and A. Surprenant P2X7 Receptor Differentially Couples to Distinct Release Pathways for IL-1{beta} in Mouse Macrophage J. Immunol., June 1, 2008; 180(11): 7147 - 7157. [Abstract] [Full Text] [PDF] Y. Qu, L. Franchi, G. Nunez, and G. R. Dubyak Nonclassical IL-1beta Secretion Stimulated by P2X7 Receptors Is Dependent on Inflammasome Activation and Correlated with Exosome Release in Murine Macrophages J. Immunol., August 1, 2007; 179(3): 1913 - 1925. [Abstract] [Full Text] [PDF]

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