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. 2012 Feb 10:3:14.
doi: 10.3389/fimmu.2012.00014. eCollection 2012.

The Role of XCR1 and its Ligand XCL1 in Antigen Cross-Presentation by Murine and Human Dendritic Cells

Richard A Kroczek  1 , Volker Henn
Affiliations

The Role of XCR1 and its Ligand XCL1 in Antigen Cross-Presentation by Murine and Human Dendritic Cells

Richard A Kroczek et al. Front Immunol. .

Abstract

Recently, the chemokine receptor XCR1 has been found to be exclusively expressed on a subset of dendritic cell (DC) known to be involved in antigen cross-presentation. This review aims to summarize the known biology of the XCR1 receptor and its chemokine ligand XCL1, both in the mouse and the human. Further, any involvement of this receptor-ligand pair in antigen uptake, cross-presentation, and induction of innate and adaptive cytotoxic immunity is explored. The concept of antigen delivery to DC via the XCR1 receptor is discussed as a vaccination strategy for selective induction of cytotoxic immunity against certain pathogens or tumors.

Keywords: XCL1; XCR1; antigen cross-presentation; antigen targeting; dendritic cells; vaccination.

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Figures

Figure 1
Figure 1
Involvement of the XCL1–XCR1 communication axis in the innate and adaptive cytotoxic responses to cross-presented microbial and tumor antigens. Secretion of the chemokine XCL1 by activated NK cells specifically attracts XCR1-expressing DCs capable of antigen cross-presentation. This ensures an effective communication between these cells in the innate phase of the immune response. In the adaptive phase, secretion of XCL1 by activated CD8+ T cells optimizes the dialog with antigen cross-presenting DCs and facilitates the differentiation of CD8+ T cells to cytotoxic effector cells.
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References

    1. Bachem A., Güttler S., Hartung E., Ebstein F., Schaefer M., Tannert A., Salama A., Movassaghi K., Opitz C., Mages H. W., Henn V., Kloetzel P. M., Gurka S., Kroczek R. A. (2010). Superior antigen cross-presentation and XCR1 expression define human CD11c+ CD141+ cells as homologues of mouse CD8+ dendritic cells. J. Exp. Med. 207, 1273–128110.1084/jem.20100348 - DOI - PMC - PubMed
    1. Bar-On L., Birnberg T., Lewis K. L., Edelson B. T., Bruder D., Hildner K., Buer J., Murphy K. M., Reizis B., Jung S. (2010). CX3CR1+ CD8α+ dendritic cells are a steady-state population related to plasmacytoid dendritic cells. Proc. Natl. Acad. Sci. U.S.A. 107, 14745–1475010.1073/pnas.1001562107 - DOI - PMC - PubMed
    1. Blaschke S., Middel P., Dorner B. G., Blaschke V., Hummel K. M., Kroczek R. A., Reich K., Benoehr P., Koziolek M., Muller G. A. (2003). Expression of activation-induced, T cell-derived, and chemokine-related cytokine/lymphotactin and its functional role in rheumatoid arthritis. Arthritis Rheum. 48, 1858–187210.1002/art.11171 - DOI - PubMed
    1. Bleul C. C., Fuhlbrigge R. C., Casasnovas J. M., Aiuti A., Springer T. A. (1996). A highly efficacious lymphocyte chemoattractant, stromal cell-derived factor 1 (SDF-1). J. Exp. Med. 184, 1101–110910.1084/jem.184.3.1101 - DOI - PMC - PubMed
    1. Bonifaz L., Bonnyay D., Mahnke K., Rivera M., Nussenzweig M. C., Steinman R. M. (2002). Efficient targeting of protein antigen to the dendritic cell receptor DEC-205 in the steady state leads to antigen presentation on major histocompatibility complex class I products and peripheral CD8+ T cell tolerance. J. Exp. Med. 196, 1627–163810.1084/jem.20021598 - DOI - PMC - PubMed

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