Background: Langerhans cells (LCs) are important antigen-presenting cells in the epidermis and may play a key role in the pathogenesis of psoriasis. It has been proven that LCs isolated from psoriatic lesions are abnormal. However, the mechanism of the abnormality has not been reported so far.
Objective: In the present study, we investigated the effect of psoriatic lesional keratinocytes on the maturation of LCs.
Methods: Monocytes isolated from healthy peripheral blood could differentiate into LCs in the presence of granulocyte-macrophage colony-stimulating factor, interleukin (IL) 4 and transforming growth factor beta1 for 5 days. Then, human monocyte-derived LCs were cultured with supernatants from psoriatic lesional keratinocytes for another 2 days. Their phenotypes and phagocytic capacity were analyzed by flow cytometry. IL-12 secreted by LCs was determined by ELISA.
Results: Supernatants from psoriatic lesional keratinocytes could up-regulate the expression of HLA-DR and CD86 on LCs more significantly than supernatants from healthy keratinocytes, but less powerfully than lipopolysaccharide. The levels of IL-12 secreted by LCs also increased. In contrast, the expression of CD1a on LCs and their phagocytic capacity were reduced.
Conclusion: Human monocyte-derived LCs cultured with supernatants from psoriatic lesional keratinocytes displayed the characteristics of maturation. This suggests that psoriatic lesional keratinocytes might secrete some factors that could promote the maturation of LCs, which may play important roles in immune reactions related to psoriasis.
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