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Characterization of Myeloid and Plasmacytoid Dendritic Cells in Human Lung¹

Barbara J. Masten^2,*, Gwyneth K. Olson^2,*, Christy A. Tarleton^*, Chad Rund^*, Mark Schuyler, Reza Mehran^3,, Tereassa Archibeque and Mary F. Lipscomb^*,4

^* Departments of Pathology, Department of Internal Medicine, and Department of Surgery, University of New Mexico, Albuquerque, NM 87131

Dendritic cells (DCs) are bone marrow-derived mononuclear cells that play a central role in the initiation of immune responses. Because human lung DCs have been incompletely characterized, we enumerated and phenotyped mononuclear cell populations from excess lung tissue obtained at surgery. Myeloid DCs (MDCs) were identified as CD1c⁺CD11c⁺CD14^–HLA-DR⁺ cells and comprised 2% of low autofluorescent (LAF) mononuclear cells. Plasmacytoid DCs (PDCs) were characterized as CD123⁺CD11c^–CD14^–HLA-DR⁺ cells and comprised 1.0% of the LAF mononuclear cells. Cells enriched in MDCs expressed CD86, moderate CD80, and little CD40, but cells enriched in PDCs had little to no expression of these three costimulatory molecules. CD11c⁺CD14^– lineage-negative (MDC-enriched) LAF cells were isolated and shown to be much more potent in stimulating an alloreaction than CD11c⁺CD14⁺ lineage-negative (monocyte-enriched) LAF cells. PDC-enriched cells were more capable of responding to a TLR-7 agonist by secreting IFN- than MDC-enriched cells. MDC-enriched cells were either CD123⁺ or CD123^–, but both subsets secreted cytokines and chemokines typical of MDC upon stimulation with a TLR-4 agonist and both subsets failed to secrete IFN- upon stimulation with a TLR-7 agonist. By immunohistochemistry, we identified MDCs throughout different anatomical locations of the lung. However, our method did not allow the localization of PDCs with certainty. In conclusion, in the human lung MDCs were twice as numerous and expressed higher levels of costimulatory molecules than PDCs. Our data suggest that both lung DC subsets exert distinct immune modulatory functions.

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 was supported by the National Institutes of Health through National Heart, Lung, and Blood Institute Grant P50-HL56384 and National Institute of Allergy and Infectious Diseases Grant U19-AI5234.

² B.J.M. and G.K.O. contributed equally to this work.

³ Current address: Department of Thoracic and Cardiovascular Surgery, University of Texas, M. D. Anderson Cancer Center, Houston, TX 77030.

⁴ Address correspondence and reprint requests to Dr. Mary F. Lipscomb, Department of Pathology, MSCO8-4640, 1 University of New Mexico, Albuquerque, NM 87131-0001. E-mail address: mlipscomb{at}salud.unm.edu

⁵ Abbreviations used in this paper: DC, dendritic cell; BDCA, blood DC Ag; HAF, high autofluorescent cell; LAF, low autofluorescent cell; MDC, myeloid DC; MFI, mean fluorescence intensity; MOI, multiplicity of infection; PDC, plasmacytoid DC.

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