Studies on the plasma membrane of normal and psoriatic keratinocytes. 5. Lectin binding

Abstract

The glycocalyx of epidermal keratinocytes from psoriatic patients has been investigated by means of lectins. Striking changes were found in the levels of glucose and/or mannose (concanavalin A) and of N-acetylglucosamine and/or sialic acid (wheat germ agglutinin) on the surface of cells from the psoriatic lesion. Smaller but significant changes were seen in the clinically uninvolved epidermis of the patient. A marked increase in the affinity of the cell surface for Ulex europus agglutinin (fucose-specific) confirms our previous reports of structural alterations in fucose-containing oligosaccharides in psoriasis.

Effect of retinoic acid and low calcium conditions on surface glycoconjugates defined by differential lectin labelling in mouse epidermal cell culture

“…The findings correlated with the pattern in whole adult mouse skin (Table i) where the various antigens are characteristic of progressively more differentiated cells (Brabec et ai, 1980;Nemanic & Elias, 1979;Brysk & Snider, 1982). Thus, irrespective of other characteristics of primary mouse epidermal cell cultures, the cell surface glycoconjugates seem to be similar to those occurring in whole epidermis, just as the cell surface glycoconjugates of human primary cell suspensions (Gommans & van den Hurk, 1981) were similar to those in whole human epidermis (Gommans & van den Hurk, 1982). Arrest or delay of differentiation by either retinoids or calcium deprivation prevented or greatly diminished the orderly appearance of A'-acetyl-galactosamine, fucose, and iV-acetyl-glucosaminc on the cell surface.…”

“…The intensity of staining and sharpness ofthe ends ofthe range of specificity for cell layers varies with each agent used. As has been shown by others (Brabec et ai, 1980;Gommans & van den Hurk, 1982;Nemanic & Elias, 1979;Stanley et ai, 1980;Podolsky & Weiser, 1973). BP and Ric.…”

Altered binding of Ulex europaeus I lectin to psoriatic epidermis

“…Enzymatically isolated keratinocytes from normal skin and from both diseased and uninvolved psoriatic epidermis also appear to bind UEA I lectin (Gommans et al, 1982). However, contradictory results on binding of UEA I to epidermal cells have also been reported: Reano et al,(i982a,b) did not find any binding of UEA I lectin to either normal or psoriatic epidermis.…”

“…Psoriatic keratinocytes appear to have altered surface properties (Orfanos ei al., 1973;Gommans et al, 1979), which could partly explain the disturbances in cell proliferation and differentiation found in the disease (Mahrle & Orfanos, 1977). Changes in labelling with radioactive sugars (Roelfzema et al, 1981) in binding of some lectins (Gommans et al, 1982) and also specific surface glycoprotein alterations (Kariniemi, Lehto & Virtanen, 1983) have been found in epidermal cells in psoriasis.…”

“…Studies on rodent epidermis with fluorochrome-coupled lectins have 524 A.-L. Kariniemi et al revealed that some lectins bind to distinct layers of epidermis (Brabec et al, 1980). Results on human skin have been more confiicting (Holt, Hill Anglin & Nordquist, 1979;Reano et al, 1982a,b) but it appears that psoriatic epidermal cells show alterations at least in binding of some a-fucosyl-specific lectins, such as Ulex europaeus agglutinin I (UEA I) (Gommans et al, 1982). In this respect it is interesting that in line with results on rodent epidermis (Brabec et al, 1980) UEA I lectin appears to react selectively with the upper Malpighian and granular cell layers of normal human epidermis in addition to dermal vascular endothelium (Holthofer et al, 1982).…”