Peripheral blood natural killer (NK) cells are usually defined as a homogeneous cell population. However, NK cells show heterogeneous expression of a diversity of cell surface molecules, which might reflect the diversity of NK-cell functions. Therefore, a more specific phenotypic definition of NK cells is necessary. In this study, we made an inventory of phenotypic subsets that are present within the peripheral blood NK-cell population of healthy donors based on differential expression of nine cell-surface markers. Using threecolour flow cytometric analysis we were able to define at least 48 different CD56 1 NK-cell subsets within the peripheral blood. This phenotypic heterogeneity appeared to be stable among healthy individuals, and was also steady within CD56 dim and CD56 bright NK populations, indicating a possible role for these subsets in NK-cell function or differentiation.

Aim: The aim of the study was to investigate changes in cell adhesion molecule expression in human lens epithelial cells (HLEC) subjected to glucocorticoids.Methods: Human lens epithelial cells were exposed to different concentrations of dexamethasone for 24 hours. Cell adhesion molecule expression was studied by western blot and immunohistochemistry of vimentin, N-cadherin, E-cadherin, α-catenin, β-catenin and γ-catenin. Expression of the glucocorticoid receptor (GR) was also studied. Cell morphology was examined by transmission electron microscopy (TEM).Result:Expression of N-cadherin, α-catenin, β-catenin and GR was significantly decreased in dexamethasone exposed cells as compared to unexposed cells. No significant change in γ-catenin was present. Visualization of adhesion molecules, N-cadherin and α-catenin, by immunohistochemistry showed decreased antigen reactivity in dexamethasone exposed as compared to the unexposed cells. However, no change was seen for β-catenin and γ-catenin. E-cadherin was not detectable using western blot or immunohistochemistry.TEM showed multilayering of cells, vacuole formation and appearance of electron-dense multivesicular bodies in HLEC exposed to 0, 0.1, 1, 10 and 100 αM dexamethasone.Conclusion:Glucocorticoids affect several adhesion molecules in lens epithelial cells, something that may contribute to the pathogenesis of posterior subcapsular opacification.

In the present study, the nature of hyperacute xenograft rejection was closely studied in a vascularized mouse-to-rat transplantation model. Antibodies against mouse heart, erythrocytes and lymphocytes and against the Forssman antigen were raised in the rat. Upon heterotopic heart transplantation the respective antisera were intravenously (i.v.) injected. Passive transfer of antiheart, antierythrocyte or antilymphocyte serum resulted in hyperacute rejection of the transplanted mouse heart. Subfractionation of the antiheart serum showed that the capacity to induce hyperacute rejection was carried by the immunoglobulin (Ig)G fraction. When antierythrocyte serum adsorbed with mouse erythrocytes was administered the cardiac grafts remained beating. To the contrary, antilymphocyte serum adsorbed with erythrocytes still had the capacity to induce hyperacute rejection. None of the rats that had previously been challenged with the Forssman antigen rejected their grafts hyperacutely. Subsequent investigations by electron microscopy revealed that the Forssman antigen is expressed on dendritic cells (DC) adjacent to the vessels, but not on the vascular endothelium, thus explaining the inability of the anti-Forssman serum to induce hyperacute rejection. Taken together, we have demonstrated the existence of several xenoantigens that can be targets for antibodymediated rejection, suggesting that more than one relevant xenoantigen exists also in more distantly related combinations, such as the pig-to-human combination.

Purpose The aim of the study was to investigate changes in cell adhesion molecule expression in human lens epithelial cells subjected to glucocorticoids. Methods Human lens epithelial cells (HLEC) were exposed to dexamethasone for 24 hours. Cell morphology was examined by transmission electron microscopy (TEM), cell adhesion molecule expression was studied by western blot and immuno‐histochemistry. Results TEM showed multilayering of cells, vacuole formation and appearance of electron‐dense multivesicular bodies in HLEC exposed to 0.1, 1, 10 and 100 µM dexamethasone. Western blot and densitometry analysis revealed that α‐catenin, β‐catenin and GR expression were significantly decreased in dexamethasone exposed HLEC compared to unexposed cells. No significant change in N‐cadherin, γ‐catenin or vimentin expression between dexamethasone exposed and unexposed cells were present. Immunohistochemical analysis showed no significant change in antigen expression for any of the antigens examined. Conclusion The multilayering of HLEC seen with TEM, indicate defects in regulation of cell migration, which is supported by a decrease in cell adhesion molecule expression.