After antigen uptake in the epidermis, LCs migrate into the T-cell areas of the lymph nodes, where they present their antigens to the T cells. The considerable changes in the immunophenotype, which occur during this migration in vivo, may be studied in vitro by investigating freshly isolated cells during short-term culture (Romani et al. 1989). Although LCs lose their characteristic BG and CD1a expression, several other surface molecules required for the initiation of immune responses are expressed de novo. This involves the up-regulation of MHC class I and II molecules, of adhesion molecules (e. g., intercellular adhesion molecule-1), and of co-stimulatory molecules such as CD80 and CD86 (Romani et al. 1989, Schuller et al. 2001,Teunissen et al. 1990).

LCs may play a role in the pathogenesis of LE (Bos et al. 1986, Mori et al. 1994, Sontheimer and Bergstresser 1982), atopic dermatitis (Bruynzeel-Koomen et al. 1986), allergic contact eczema (Silberberg et al. 1973), psoriasis vulgaris (Bos et al. 1983), and mycosis fungoides (Pimpinelli et al. 1994) by presentation of (auto)antigens to T cells.

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