Glycophenotype of psoriatic skin

Psoriasis is considered an auto-immune disease with consequential keratinocyte hyperproliferation resulting in specific architecture of psoriatic skin. This process is associated with phenotypical keratinocyte changes including an altered carbohydrate expression pattern studied by labelled plant lectins. Expression of endogenous lectins and their reactive glycoligands are differentiation-dependent in squamous epithelia including epidermis. However, no data are available on psoriatic skin, although this disease represents an important medical problem. We investigated the expression of galectin-1, -3, -7 and the presence of their glycoligands in the psoriatic skin and compared the results with the normal skin samples. The results were correlated to expression patterns of cytokeratin 10 and cytokeratin peptide 37 as markers of keratinocyte differentiation as well as to the expression of proliferation marker Ki67. Contrary to normal epidermis, the psoriatic epithelium expressed no galectin-3 and no glycoligands for galectin-1. Strong expression of galectin-3/galectin-3-reactive glycoligands in capillaries of psoriatic dermis represents one of the most important findings demonstrating the activation of endothelium in the course of the disease. The keratin expression pattern was not affected in psoriatic skin compared with normal epidermis. In conclusion, the altered galectin expression and binding pattern in psoriatic skin indicates the modified process of keratinocyte maturation in hyperactivated psoriatic epithelium. The enhanced expression of galectin-3/galectin-3-reactive glycoligands in dermal capillaries of psoriatic skin can be important for rearrangement of the capillary network and migration of inflammatory cells to psoriatic skin.