PDCs may induce Th1- or Th2-predominated immune responses. In the presence of IL-3 and CD40 ligand, PDCs develop into mature DCs and induce naive T cells to produce Th2 cytokines (Rissoan et al. 1999). On the other hand, virus-triggered PDCs can induce a Th1 response by activating naive CD4+ T cells to produce IFN-y and IL-10 (Cella et al. 2000, Kadowaki et al. 2000). Thus, PDCs may play an important role in several inflammatory skin diseases.

Patients with LE have high systemic IFN-a levels that are associated with disease activity. PDCs have been proposed to be the main source of IFN-a in LE (Kim et al. 1987). Anti-double-stranded DNA antibodies in combination with immunostimula-tory plasmid DNA mimic an endogenous IFN-a inducer in SLE (Vallin et al. 1999). PDCs have been found to produce IFN-a in response to plasmid DNA/anti-DNA-antibody complexes (Dzionek et al. 2001).

Considering the many immunoregulatory actions of IFN-a, prolonged endogenous production of this cytokine may be an important pathogenic factor in LE. Although IFN-y modulates several immunologic processes, including inhibiting the granulocyte macrophage-colony-stimulating factor-induced expression of CD80 on LCs (Ozawa et al. 1996), it is not yet clear whether high levels of IFN-a may also have a direct effect on LCs. Although IFN-a-induced LE has not yet been described, SLE-like syndrome has been reported in a patient with malignant carcinoid tumor undergoing IFN-a therapy (Ronnblom et al. 1990).

High IL-10 levels, which may be secreted by PDC-stimulated CD4+ T cells, may also prevent the maturation of monocytes into DCs (Allavena et al. 1998).

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