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Plasmacytoid dendritic cells (pDCs) are a subset of dendritic cells. They resemble plasma cells when viewed under a microscope and are distinct from conventional dendritic cells in terms of their development and function. pDCs produce large amounts of interferons – proteins that are important for immunity to viruses.
Dalod and colleagues utilize a combinatorial genetic reporter strategy to uniquely mark plasmacytoid dendritic cells (pDCs) in mice. They utilize these mice to identify bona fide pDCs and functionally characterize before and during viral infection, in comparison to several other DC types.
Zinc finger proteins are involved in the resolution of immune responses and function by degrading mRNA of inflammatory cytokines. Here the authors show MCPIP3 promotes skin inflammation via modification of cytokine profiles in pDCs and macrophages.
Type I interferon drives autoimmune pathology in SLE and has been assumed to come predominantly from plasmacytoid dendritic cells (pDCs). Here, the authors show that prior to the onset of SLE, pDCs lose multiple immunogenic functions and, instead, non-hematopoietic cells such as keratinocytes are a major source of type I interferons.
Confusion exists as to whether transitional dendritic cells are a bone fide subset or just a transitional state, as the name indicates. New data are complicating matters further by showing some interesting heterogeneity in these cells.
Taking advantage of intersectional genetics, Valente et al. report a novel strategy for tracking plasmacytoid dendritic cells (DCs) that enables their discrimination from conventional DCs and plasmacytoid DC–like cells, as well as transitional DCs.
Emerging data suggest a lymphoid origin of plasmacytoid dendritic cells (pDCs), which, in most cases, do not share the classical functional properties of myeloid dendritic cells. This Comment proposes that pDCs should be assigned to a subcategory of innate lymphocytes and should be referred to as interferon-producing cells.
New research attempts to explore the cause of plasmacytoid dendritic cell hyperactivation in systemic lupus erythematosus by focusing on genetic risk variation.
