Contaminating Factor(s). Importantly, R-hcg Stimulated-il-8

production by PBMC is mediated not through LH/hCG receptor, but through glucose receptor. Therefore, it should be noted that the response of PBMC to hCG might depend on the glycosylation status of hCG reagent(s) (Kosaka et al., 2002). We also observed that r-hCG-stimulated PBMC effectively promote invasion of murine and human trophoblastic cells by producing bioactive molecules (Egawa et al., 2002; Nakayama et al., 2002), suggesting that hCG affects PBMC function to facilitate embryo implantation (Fujiwara, 2006). In addition, we preliminarily observed that r-hCG promoted vascular endothelial growth factor (VEGF) production by PBMC (unpublished data). Accordingly, taken together with our recent findings (Kosaka et al., 2007), we think it is possible that immune cells produce VEGF and contribute to increased capillary permeability in OHSS. Very recently, it was reported that r-hCG induced indoleamine 2,3-dioxygenase expression in dendritic cells, which in turn inhibited the activation of diabetogenic CD4(þ) and CD8(þ) T-cells in mice (Ueno et al., 2007). Therefore, we think that analysis of the direct effects of hCG on immune system should be continued in the future.