Summary Macrophages/monocytes and the proinflammatory mediators, such as tumour necrosis factor (TNF)‐α, prostaglandin E2 (PGE2), macrophage inflammatory protein (MIP)‐1α and MIP‐1α, play a critical role in the progression of immunological disorders including rheumatoid arthritis, Behçet’s disease and Crohn’s disease. In addition, the nicotinic acetylcholine receptor‐α7 (α7nAChR) subunit is an essential regulator of inflammation. In this study, we evaluated the expression of the α7nAChR subunit on human peripheral monocytes and the effect of nicotine on the production of these proinflammatory mediators by activated monocytes. Fluorescein isothiocyanate (FITC)‐labelled α‐bungarotoxin demonstrated the cell surface expression of the α7nAchR subunit. Pretreatment with low‐dose nicotine caused inhibition of TNF‐α, PGE2, MIP‐1α and MIP‐1α production, and mRNA expression of TNF‐α, MIP‐1α and MIP‐1α and COX‐2 in lipopolysaccharide (LPS)‐activated monocytes. These suppressive effects of nicotine were caused at the transcriptional level and were mediated through α7nAChR. Nicotine suppressed the phosphorylation of I‐κB, and then inhibited the transcriptional activity of nuclear factor‐κB. These immunosuppressive effects of nicotine may contribute to the regulation of some immune diseases.

Summary Involvement of excessive

This study demonstrates that CDDP specifically induces apoptosis via activation of caspases and the other anticancer drugs induce death of HOS cells via different signaling pathways. It also demonstrates that caspase-8 is a key molecule in the earliest stage of the signaling pathway of CDDP-induced apoptosis of HOS cells, and caspase-3 works downstream of caspase-8.

Epithelial progenitors were successfully induced in vitro from ES cells and were applicable as grafts for treating corneal epithelial injury. ES cells may become an unlimited donor source of corneal epithelial cells for corneal transplantation and may restore useful vision in patients with a deficiency of limbal epithelial cells. This is an important first trial toward assessing the use of ES cells to reconstruct corneal epithelial cells.

SummaryExcessive T helper type 1 (Th1) cell activity has been reported in Behçet's disease (BD). Recently, association of Th17 cells with certain autoimmune diseases was reported, and we thus investigated circulating Th17 cells in BD.