The simultaneous expression of cell surface antigens and intracellular IFN-a in herpes simples virus-stimulated PDCs was examined by flow cytometry. PDCs were confirmed to lack leukocyte lineage-specific markers and to express CD4, CD36, and HLA-DR (Svensson et al. 1996). Furthermore, high levels of CD44, CD45RA, and CD45RB and moderate levels of CD40, CD45R0, CD72, and CD83 were detected. Expression of CD13, CD33, and FceRI was weak, whereas no CD5, CD 11b, CD 16, CD64, CD80, or CD86 was detected at all (Svensson et al. 1996). Today it is clear that the immunophenotype of PDCs somewhat resembles that of immunoglobulin-secreting plasma cells. Common gating strategies for PDCs from peripheral blood are based on a class II-positive (HLA-DR+), lineage-negative (CD3-, CD14-, CD16-, CD19-, CD20-, CD56-), interleukin (IL)-3 receptor a-chain-positive (CD123+), CD11 c- cell population (Wollenberg et al. 2002).

In skin sections of patients with discoid LE and SLE, PDCs are easily identified by their high expression of CD123 and HLA-DR and co-expression of CD45RA and CD68 (Farkas et al. 2001). The density of PDCs correlates with the presence of a high number of cells expressing the IFN-a- and IFN-ß-inducible protein MxA (Farkas et al. 2001).

Flow cytometric detection of PDCs from different inflammatory skin lesions has recently been described and may be performed by gating strategies for either HLA-DR+, lineage-negative, CD123+, CD11 c-negative cells or for HLA-DR+, lineage- negative, BDCA-2-positive cells (Wollenberg et al. 2002). The BDCA-2 antibody is directed against a recently identified C-type lectin, which is expressed weakly but very specifically on PDCs in peripheral blood and inflamed skin (Dzionek et al. 2001).

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