Results of the present study confirm the hypothesis of impaired T-cell-mediated immunity after allogeneic transfusion.

~~Fusion between monocytes and tumor cells has been suggested as a cause for tumor metastasis. The aim of the present study was to establish an in vitro fusion model representing the in vivo situation as close as possible. For this purpose fusion between cells was induced by cytokine containing conditioned medium. In order to prove that hybrid formation between tumor cells and monocytes occurs, a two-color-fusion-assay based on membrane labeling with the fluorochromes PKH 2 (green) and PKH 26 (red) was established. These fusion experiments were analyzed by microscopy and, in addition, by flow cytometry. The attempt to induce fusion between monocytes and several tumor cell lines of hematopoietic origin revealed quite diverse results.-

Multinucleated giant cells (MGC) are a common feature of granulomas that develop during various inflammatory reactions. MGC originate from fusion of monocytes or macrophages, but the exact mechanism of their generation is still unclear. In the present study, we investigated the influence of monocyte to macrophage maturation on the ability of human monocytes/macrophages to fuse with each other. MGC were generated in vitro by stimulation of human peripheral blood monocytes with cytokine containing supernatants. With freshly isolated monocytes, fusion rates of up to 90% were obtained. When monocyte to macrophage maturation was induced by culturing the cells in human serum, fusion rates gradually decreased with advancing time of the preceding culture (corresponding to the stage of differentiation) and almost no MGC formation could be obtained with 8-day-old macrophages. In contrast, fusion rates did not decrease when monocytes had been cultured under serum free conditions before stimulation. When freshly isolated monocytes were added to 1-week cultured macrophages, which had been membrane-labeled with a fluorochrome, fusion between the two populations could be induced. Because the ability for intracellular killing of certain pathogens is reduced in macrophages, fusion with monocytes (newly arriving at the site of inflammation) may represent an attempt to restore this capacity.

The pseudohyphal form of Candida albicans is able to bind iC3b. This may play an important role in the pathogenesis of disseminated candidiasis and, in particular, in adherence to endothelium, protection against complement action, and iron acquisition from erythrocytes. Here we report that Ca2+ ions are required to maintain stable binding of iC3b to C. albicans pseudohyphae.

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