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      Superior antigen cross-presentation and XCR1 expression define human CD11c +CD141 + cells as homologues of mouse CD8 + dendritic cells

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          In recent years, human dendritic cells (DCs) could be subdivided into CD304 + plasmacytoid DCs (pDCs) and conventional DCs (cDCs), the latter encompassing the CD1c +, CD16 +, and CD141 + DC subsets. To date, the low frequency of these DCs in human blood has essentially prevented functional studies defining their specific contribution to antigen presentation. We have established a protocol for an effective isolation of pDC and cDC subsets to high purity. Using this approach, we show that CD141 + DCs are the only cells in human blood that express the chemokine receptor XCR1 and respond to the specific ligand XCL1 by Ca 2+ mobilization and potent chemotaxis. More importantly, we demonstrate that CD141 + DCs excel in cross-presentation of soluble or cell-associated antigen to CD8 + T cells when directly compared with CD1c + DCs, CD16 + DCs, and pDCs from the same donors. Both in their functional XCR1 expression and their effective processing and presentation of exogenous antigen in the context of major histocompatibility complex class I, human CD141 + DCs correspond to mouse CD8 + DCs, a subset known for superior antigen cross-presentation in vivo. These data define CD141 + DCs as professional antigen cross-presenting DCs in the human.

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          Most cited references 36

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          Taking dendritic cells into medicine.

          Dendritic cells (DCs) orchestrate a repertoire of immune responses that bring about resistance to infection and silencing or tolerance to self. In the settings of infection and cancer, microbes and tumours can exploit DCs to evade immunity, but DCs also can generate resistance, a capacity that is readily enhanced with DC-targeted vaccines. During allergy, autoimmunity and transplant rejection, DCs instigate unwanted responses that cause disease, but, again, DCs can be harnessed to silence these conditions with novel therapies. Here we present some medical implications of DC biology that account for illness and provide opportunities for prevention and therapy.
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            Human and mouse plasmacytoid dendritic cells have been shown to correspond to a specialized cell population that produces large amounts of type I interferons in response to viruses, the so-called natural interferon-producing cells. As a result, intensive investigation is now focused on the potential functions of plasmacytoid dendritic cells in both innate and adaptive immunity. Here we review recent progress on the characterization of plasmacytoid dendritic cell origin, development, migration and function in immunity and tolerance, as well as their effect on human diseases.
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              IPC: professional type 1 interferon-producing cells and plasmacytoid dendritic cell precursors.

               Yong-feng Liu (2004)
              Type 1 interferon-(alpha, beta, omega)-producing cells (IPCs), also known as plasmacytoid dendritic cell precursors (pDCs), represent 0.2%-0.8% of peripheral blood mononuclear cells in both humans and mice. IPCs display plasma cell morphology, selectively express Toll-like receptor (TLR)-7 and TLR9, and are specialized in rapidly secreting massive amounts of type 1 interferon following viral stimulation. IPCs can promote the function of natural killer cells, B cells, T cells, and myeloid DCs through type 1 interferons during an antiviral immune response. At a later stage of viral infection, IPCs differentiate into a unique type of mature dendritic cell, which directly regulates the function of T cells and thus links innate and adaptive immune responses. After more than two decades of effort by researchers, IPCs finally claim their place in the hematopoietic chart as the most important cell type in antiviral innate immunity. Understanding IPC biology holds future promise for developing cures for infectious diseases, cancer, and autoimmune diseases.

                Author and article information

                J Exp Med
                J. Exp. Med
                The Journal of Experimental Medicine
                The Rockefeller University Press
                7 June 2010
                : 207
                : 6
                : 1273-1281
                [1 ]Molecular Immunology, Robert Koch-Institute, 13353 Berlin, Germany
                [2 ]Institute of Biochemistry, Charité University Hospital, Humboldt University, 10117 Berlin, Germany
                [3 ]Rudolf-Boehm-Institute of Pharmacology and Toxicology, 04107 Leipzig, Germany
                [4 ]Institute of Transfusion Medicine, Charité University Hospital, Humboldt University, 13353 Berlin, Germany
                Author notes
                CORRESPONDENCE Richard A. Kroczek: kroczek@

                A. Bachem, S. Güttler, and E. Hartung contributed equally to this paper.

                S. Gurka and R.A. Kroczek contributed equally to this paper.

                © 2010 Bachem et al.

                This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at




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