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CX₃CR1⁺c-kit⁺ Bone Marrow Cells Give Rise to CD103⁺ and CD103^– Dendritic Cells with Distinct Functional Properties¹

Maria-Luisa del Rio^*, Jose-Ignacio Rodriguez-Barbosa, Jasmin Bölter^*, Matthias Ballmaier, Oliver Dittrich-Breiholz, Michael Kracht^¶, Steffen Jung^|| and Reinhold Förster^2,*

^* Institute of Immunology, Hannover Medical School, Hannover, Germany; Institute of Biomedicine, Immunology Section, University of León, León, Spain; Clinic for Pediatric Hematology and Oncology and Institute of Biochemistry, Hannover Medical School, Hannover, Germany; ^¶ Rudolf-Buchheim Institute of Pharmacology, University of Giessen, Giessen, Germany; and ^|| Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel

Dendritic cells (DC) represent a rather heterogeneous cell population with regard to morphology, phenotype, and function and, like most cells of the immune system, are subjected to a continuous renewal process. CD103⁺ (integrin _E) DC have been identified as a major mucosal DC subset involved in the induction of tissue-specific homing molecules on T cells, but little is known about progenitors able to replenish this DC subset. Herein we report that lineage (lin)^–CX₃CR1⁺c-kit⁺ (GFP⁺c-kit⁺) bone marrow cells can differentiate to either CD11c⁺CD103^– or CD11c⁺CD103⁺ DC in vitro and in vivo. Gene expression as well as functional assays reveal distinct phenotypical and functional properties of both subsets generated in vitro. CD103^– DC exhibit enhanced phagocytosis and respond to LPS stimulation by secreting proinflammatory cytokines, whereas CD103⁺ DC express high levels of costimulatory molecules and efficiently induce allogeneic T cell proliferation. Following adoptive transfer of GFP⁺c-kit⁺ bone marrow cells to irradiated recipients undergoing allergic lung inflammation, we identified donor-derived CD103⁺ DC in lung and the lung-draining bronchial lymph node. Collectively, these data indicate that GFP⁺c-kit⁺ cells contribute to the replenishment of CD103⁺ DC in lymphoid and nonlymphoid organs.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work has been supported by Deutsche Forschungsgemeinschaft Grant SFB587-B3 to R.F.

² Address correspondence and reprint requests to Dr. Reinhold Förster, Institute of Immunology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany. E-mail address: foerster.reinhold{at}mh-hannover.de

³ Abbreviations used in this paper: DC, dendritic cell; BALF, bronchoalveolar lavage fluid; brLN, bronchial lymph node; eGFP, enhanced GFP; lin, lineage; LN, lymph node; MDP, macrophage and DC progenitor; PI, propidium iodide; PRR, pattern recognition receptor; SR, scavenger receptor.

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