SUMMARYHuman monocyte-derived macrophages have been proposed as agents of anti-tumour immunotherapy. The aim of the present study was to investigate in vitro the properties of these cells likely to control their recruitment to the sites of inflammation and tumours. The expression of adhesion molecules involved in the binding of monocytes to endothelial cells was modified during monocyte-macrophage differentiation, with a significant increase in CD11c, CD14 and intercellular adhesion molecule-1 (ICAM-1). Monocyte-derived macrophages were sensitive to chemoattractants, in particular to the monocytespecific chemokine monocyte chemotactic protein-1 (MCP-1). They responded by an increased expression of adhesion molecules and were attracted by the cytokine in an under-agarose migration assay. The migration response, however, decreased after days 4-5 of monocyte differentiation into macrophage. In conclusion, human monocyte-derived macrophages show alterations of surface structures involved in the recognition of inflammatory endothelium. This may explain why the cells are poorly recruited to the sites of inflammation and tumours when introduced into the circulation.

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In this study, we assessed the LFA‐1 (CD18/CD11a) and CR3 (CD18/CD11b) expression on peripheral polymorphonuclear leukocytes (PB‐PMN) and crevicular fluid polymorphonuclear leukocytes (CF‐PMN), by subjects with a healthy periodontium (n=1), gingivitis (n=8). early‐onset periodontitis (n=17) and adult periodontitis (n=8). Using flow cytometry analysis, the %s of CD18, CD11a and CD11b positive cells and the absolute numbers of fluorescent molecules were determined. No significant difference could be found among the 4 groups, for these 2 kinds of parameters, in PB‐PMN or CF‐PMN. However, a great difference could be noted between the results obtained from PB‐PMN and those obtained from CF‐PMN. The %s of positive CF‐PMN were significantly lower than those of PB‐PMN for the 3 sub‐units (p < 0.001). The levels of CD18 and CD11b expressed by CF‐PMN were higher than those expressed by PB‐PMN and the difference was significant for CD11b (p < 0.001). On the contrary, the level of CD11a expressed on CF‐PMN was significantly lower than that expressed by PB‐PMN (p < 0.001). Hence, our current results show that early‐onset periodontitis PMN can be quite normal and this fact is not surprising insofar as, in our study, these cells were perfectly functional and all the subjects were in good health. We concluded that the analysis of the leukocyte adhesion receptors expression on PB‐PMN does not appear useful for helping to establish a differential diagnosis between the different forms of periodontitis. However, the pattern of expression study on CF‐PMN may permit a better comprehension of the local phenomena which are implicated in the defence of the periodontal tissues against oral microorganisms.