Deficiency of Plasmacytoid DCs in AD

Plasmacytoid DCs are CD1a negative as well as CD11c negative but positive for the a-chain of the IL-3 receptor (CD123) and the blood-dendritic cell antigen (BDCA)-2. They are equipped with specific pattern recognition receptors of the innate immune system which enable them to sense microbial pathogens and thereby defend our organism against bacterial and viral infections (Soumelis and Liu 2006). Plasmacytoid DCs in the peripheral blood of AD patients have been shown to bear the FceRI receptor on their surface which is densely occupied with IgE molecules (Novak et al. 2004a). IgE receptor expression of pDC correlates with the IgE serum levels, indicating that IgE in the micromilieu might be necessary to stabilize this structure on the cell surface of pDC. Further on, activation of FceRI on pDC counter-regulates the toll-like receptor (TLR)-9 pathway involved in the regulation of the type I IFN production, which is required for the defence against virus infections (Schroeder et al. 2005). Aggregation of FceRI on pDC induces the release of IL-10 and increases in an endogenous loop IL-10-mediated apoptosis of pDC in vitro. Further on, the pre-activation of pDC via allergen challenge significantly reduces the capacity of pDC to produce IFN-a and IFN-p in response to subsequent stimulation with viral DNA motifs (Novak et al., 2004a). The reduced capacity of pDC to produce type I IFN after allergen challenge might be one of the reasons for the high susceptibility of AD patients to viral infections. There is also evidence for a reduced amount of pDC in the epidermis of AD patients in comparison to other chronic inflammatory skin diseases such as psoriasis, allergic contact dermatitis, or lupus erythematodes which might be based on a lower recruitment of these cells into the skin due to reduced expression of skin homing molecules on pDC of atopic donors or a higher rate of apoptosis of pDC in the Th2-prone micromilieu of AD skin (Wollenberg et al. 2002). The Th2-predominated immune state (Wollenberg et al. 2003; Novak and Peng 2005), modifications on the level of pDC together with other deficiencies of the innate immune system, for instance, reduced amounts of antimicrobial peptides such as cathelicidin in the skin of AD patients (Ong et al. 2002; Howell et al. 2006) have been identified as important risk factors for the manifestation of bacterial and viral infections of the skin, which significantly aggravate the course of the disease in a subgroup of AD patients.

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