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Blood, 15 March 2004, Vol. 103, No. 6, pp. 2187-2195. Prepublished online as a Blood First Edition Paper on November 6, 2003; DOI 10.1182/blood-2003-08-2729. This Article Full Text (PDF) All Versions of this Article: 2003-08-2729v1 103/6/2187    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 Wilson, N. S Articles by Villadangos, J. A Search for Related Content PubMed PubMed Citation Articles by Wilson, N. S Articles by Villadangos, J. A Social Bookmarking                   What's this? Submitted August 13, 2003 Accepted November 1, 2003 Dendritic cells constitutively present self antigens in their immature state in vivo, and regulate antigen presentation by controlling the rates of MHC class II synthesis and endocytosis Nicholas S Wilson, Dima El-Sukkari, and Jose A Villadangos* Department of Immunology, The Walter and Eliza Hall Institute, Parkville, VIC, Australia; The Cooperative Research Center for Vaccine Technology, Parkville, VIC, Australia * Corresponding author; email: villadangos{at}wehi.edu.au. Dendritic Cells (DC) change their antigen presenting properties during maturation. Immature DC efficiently capture antigens, but are reported to be impaired in their processing and presenting capacity. Upon encounter with an inflammatory stimulus, DC undergo a maturation process that leads to efficient presentation of antigens captured at the time of activation, but precludes processing of antigens encountered at later time points. The mechanisms that underlie these developmental changes are controversial. Thus, it is unclear whether immature DC can present self antigens, and which are the checkpoints that regulate antigen presentation in immature and mature DC. We have characterized these mechanisms using DC derived directly from lymphoid organs. Immature DC constitutively presented self peptide-MHC II complexes, but these were degraded quickly after their transient expression on the cell surface. During maturation, MHC II endocytosis was down-regulated, so that newly generated MHC II-peptide complexes accumulated on the plasma membrane. Simultaneously, MHC II synthesis was down-regulated, thus preventing the turn-over of the MHC II-peptide complexes that accumulated early during maturation. Our results demonstrate that immature DC constitutively present self antigens in the lymphoid organs and characterize the molecular basis of the capacity of DC to provide "antigenic memory" in vivo. 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