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      The CD8 + Dendritic Cell Subset Selectively Endocytoses Dying Cells in Culture and In Vivo

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          Abstract

          Dendritic cells (DCs) are able in tissue culture to phagocytose and present antigens derived from infected, malignant, and allogeneic cells. Here we show directly that DCs in situ take up these types of cells after fluorescent labeling with carboxyfluorescein succinimidyl ester (CFSE) and injection into mice. The injected cells include syngeneic splenocytes and tumor cell lines, induced to undergo apoptosis ex vivo by exposure to osmotic shock, and allogeneic B cells killed by NK cells in situ. The CFSE-labeled cells in each case are actively endocytosed by DCs in vivo, but only the CD8 + subset. After uptake, all of the phagocytic CD8 + DCs can form major histocompatibility complex class II–peptide complexes, as detected with a monoclonal antibody specific for these complexes. The CD8 + DCs also selectively present cell-associated antigens to both CD4 + and CD8 + T cells. Similar events take place with cultured DCs; CD8 + DCs again selectively take up and present dying cells. In contrast, both CD8 + and CD8 DCs phagocytose latex particles in culture, and both DC subsets present soluble ovalbumin captured in vivo. Therefore CD8 + DCs are specialized to capture dying cells, and this helps to explain their selective ability to cross present cellular antigens to both CD4 + and CD8 + T cells.

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          Most cited references25

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          In search of the ‘missing self’: MHC molecules and NK cell recognition

          Immunology Today, 11, 237-244
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            Dendritic cells acquire antigen from apoptotic cells and induce class I-restricted CTLs.

            CD8+ cytotoxic T lymphocytes (CTLs) mediate resistance to infectious agents and tumours. Classically, CTLs recognize antigens that are localized in the cytoplasm of target cells, processed and presented as peptide complexes with class I molecules of the major histocompatibility complex (MHC). However, there is evidence for an exogenous pathway whereby antigens that are not expected to gain access to the cytoplasm are presented on MHC class I molecules. The most dramatic example is the in vivo phenomenon of cross-priming: antigens from donor cells are acquired by bone-marrow-derived host antigen-presenting cells (APCs) and presented on MHC class I molecules. Two unanswered questions concern the identity of this bone-marrow-derived cell and how such antigens are acquired. Here we show that human dendritic cells, but not macrophages, efficiently present antigen derived from apoptotic cells, stimulating class I-restricted CD8+ CTLs. Our findings suggest a mechanism by which potent APCs acquire antigens from tumours, transplants, infected cells, or even self-tissue, for stimulation or tolerization of CTLs.
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              Natural adjuvants: endogenous activators of dendritic cells.

              Dendritic cells, the most potent antigen-presenting cells, need to be activated before they can function to initiate an immune response. We report here that, in the absence of any foreign substances, dendritic cells can be activated by endogenous signals received from cells that are stressed, virally infected or killed necrotically, but not by healthy cells or those dying apoptotically. Injected in vivo with an antigen, the endogenous activating substances can function as natural adjuvants to stimulate a primary immune response, and they may represent the natural initiators of transplant rejection, spontaneous tumor rejection, and some forms of autoimmunity.
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                Author and article information

                Journal
                J Exp Med
                The Journal of Experimental Medicine
                The Rockefeller University Press
                0022-1007
                1540-9538
                20 May 2002
                : 195
                : 10
                : 1289-1302
                Affiliations
                [1 ]Department of Animal Development and Physiology, Graduate School of Biostudies
                [2 ]Department of Zoology, Graduate School of Science, Kyoto University, Kyoto 606-8502, Japan
                [3 ]Laboratory of Cellular Physiology and Immunology, The Rockefeller University, New York, NY 10021
                Author notes

                Address correspondence to K. Inaba, Laboratory of Immunobiology, Department of Animal Development and Physiology, Division of Systemic Life Science, Graduate School of Biostudies, Kyoto University, Kitashirakawa-Oiwake-cho, Sakyo-ku, Kyoto 606-8502, Japan. Phone: 81-75-753-4088; Fax: 81-75-753-4112; E-mail: kayo@ 123456lif.kyoto-u.ac.jp

                Article
                020161
                10.1084/jem.20020161
                2193756
                12021309
                b4598efa-1cd4-4a9d-a9db-176c4252b1bb
                Copyright © 2002, The Rockefeller University Press
                History
                : 31 January 2002
                : 15 March 2002
                : 5 April 2002
                Categories
                Article

                Medicine
                cross-presentation,dendritic cell subset,dendritic cells,apoptosis,cd8+ dendritic cell
                Medicine
                cross-presentation, dendritic cell subset, dendritic cells, apoptosis, cd8+ dendritic cell

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