Unique high and homogenous surface expression of the transferrin receptor CD71 on murine plasmacytoid dendritic cells in different tissues.

Plasmacytoid dendritic cells (pDC) are of increasing interest in cancer vaccine development, but many functions of these highly specialized, multifaceted cells are poorly understood. The transferrin receptor CD71 has also been suggested to function as an antigen uptake receptor on professional antigen-presenting cells. In this study, we employed multiparameter flow cytometry to investigate CD71 expression on various leukocyte subsets, including DC subsets, granulocytes, macrophages, T and B lymphocytes, γδ T cells, and natural killer cells. Cells from various lymphoid and non-lymphoid murine tissues were analyzed using fluorochrome-conjugated monoclonal antibodies. High CD71 expression (90-100%) was observed, uniquely on pDC amongst the leukocyte populations examined, in both lymphoid and non-lymphoid tissues, including other DC subsets. In contrast, CD71 expression on non-tissue pDC, in the bone marrow and peripheral blood, was reduced. The cause and function of this high tissue pDC-selective CD71 expression remain to be examined.

Plasmacytoid dendritic cell depletion modifies FoxP3+ T cell homeostasis and the clinical course of bacterial pneumonia in mice.

Plasmacytoid dendritic cells (pDC) are critical to antiviral defense because of their high production of type I IFNs; less is known regarding their functions in bacterial infection. Moreover, pDC are involved in immunomodulation. A stable pool of regulatory T cells (Treg) is crucial for maintaining immune homeostasis. However, interactions between pDC and Treg regarding the regulation of Treg homeostasis are understudied. By using BDCA2-DTR mice as a systemic pDC depletion model, we identified increased steady-state numbers of FoxP3+ T cells with an effector Treg-like phenotype in lungs, liver, and spleen tissues. During sublethal, pulmonary Klebsiella pneumoniae infection, pDC deficiency also elevated respiratory FoxP3+ T cell numbers. Additionally, the improvement in acute pneumonia survival until day 5 post infection was accompanied by impaired proinflammatory cytokine production. In contrast, pDC-depleted mice exhibited a delayed clinical recovery during the post-acute phase. Therefore, we assume that pDC act as immunomodulators supporting the rapid onset of immune response in a proinflammatory manner and regulate inflammation or tissue regeneration in the post-acute phase. In summary, pDC assist in FoxP3+ T cell homeostasis and the regulation of Klebsiella-pneumonia progression.