Role of Kaposi's sarcoma cells in recruitment of circulating leukocytes: implications in pathogenesis.

OBJECTIVE: We sought to identify and characterize mechanisms of interaction between Kaposi's sarcoma cells and circulating leukocytes leading to leukocyte migration into the lesion. STUDY DESIGN/METHODS: By using static and dynamic adhesion models, we measured the ability of late-stage KSY1 cells to support adhesion and transmigration of peripheral blood lymphocytes (PBL). RESULTS: We showed that resting as well as TNF-alpha- or PMA-activated KSY1 cells supported adhesion and transmigration of PBL with a higher efficiency compared with normal endothelial cells. The LFA1/ICAM1 pathway was totally involved in PBL adhesion to resting or TNF-alpha-activated KSY1 cells and partially responsible for adhesion to PMA-activated KSY1 cells. No inhibition of adhesion was observed by blockage of the VLA4 pathway. Under flow conditions, PBL/KSY1 cell interaction was totally dependent on L-selectin. CONCLUSION: Our data indicate that KS cells mimic an endothelium-like structure by regulating extravasation of lymphocytes into lesions.

Quantitative analysis of leukocyte membrane antigen expression on human fetal and cord blood: normal values and changes during development.

We studied the antibody binding capacity (ABC) of various cell-surface antigens in normal human fetuses and term neonates on lymphocyte, monocyte, and polymorphonuclear (PMN) cells by quantitative flow cytometry also designated by quantimetry. Analysis of changes of expression level on these leukocytes during the developmental process was also investigated. The results indicated that the ABC values of most studied markers change during the maturational process. The ABC of lymphocyte-associated antigens studied such as CD5 and CD7 showed only a decrease from fetus to adult, whereas according to the type of molecule on monocyte and PMN there was either an increase or a decrease of ABC values dependent on the stage of the developmental process, from fetus to neonate or from neonate to adult. However, the ABC values of leukocyte membrane antigens such as CD16, CD46, and CD55 on all leukocytes and CD11b, CD11c, and CD35 on myeloid cells did not change. Their expression level was already mature in fetuses compared with adult cells. In addition, in this quantimetric approach, the analysis of the results for CD11a and CD8 suggested that the changes of CD11a expression level on lymphocyte subsets can depend on one mechanism, whereas there are probably at least two for CD8. Furthermore, the expression patterns of CD5, CD7, and CD11a change during maturation. We concluded that, even if the neonate response pattern to immunological challenge differs from an adult and this is based primarily on the relative numbers and functional activity of lymphocyte T subsets (especially TH1/TH2) and their cytokine profiles, these quantitative and qualitative phenotypical differences might also contribute to explain the functional peculiarities of leukocyte fetal and cord blood cells. All these findings support the notion of immaturity and maturity of ABC expression.