Details

Autor(en) / Beteiligte

• Hirota, Yasushi
• Osuga, Yutaka
• Koga, Kaori
• Yoshino, Osamu
• Hirata, Tetsuya
• Morimoto, Chieko
• Harada, Miyuki
• Takemura, Yuri
• Nose, Emi
• Yano, Tetsu
• Tsutsumi, Osamu
• Taketani, Yuji

Titel

The Expression and Possible Roles of Chemokine CXCL11 and Its Receptor CXCR3 in the Human Endometrium

Ist Teil von

• Journal of Immunology, 2006-12, Vol.177 (12), p.8813-8821

Ort / Verlag

United States: Am Assoc Immnol

Erscheinungsjahr

2006

Quelle

Wiley-Blackwell Full Collection

Beschreibungen/Notizen

• IFN-gamma secreted by a human embryo and trophoblast cells during implantation is suggested to play an important role in implantation and pregnancy. In the present study, we explored expression and possible functions of CXCL11, a CXC chemokine strongly induced by IFN-gamma, and its receptor CXCR3 in the human endometrium. Secreted CXCL11 protein was not detected in cultured endometrial stromal cells (ESC) but was detected in cultured endometrial epithelial cells (EEC). IFN-gamma stimulated the protein levels of CXCL11 in a dose-dependent manner in EEC and ESC. CXCL11 secreted from EEC with 100 ng/ml IFN-gamma was 220-fold of the control, and 100-fold as compared with that secreted from ESC with the same dose of IFN-gamma. CXCR3 was expressed in EEC, ESC, and trophoblast cells. Addition of IFN-gamma to EEC increased the chemotactic activity of its culture medium to trophoblast cells and T cells, and the effect was suppressed by immunoneutralization with Abs of three CXCR3 ligands, including anti-CXCL11 Ab. CXCL11 significantly increased BrdU incorporation of ESC, which was inhibited by a p42/44 MAPK pathway inhibitor PD98059. In contrast, CXCL11 significantly decreased BrdU incorporation and increased the release of lactate dehydrogenase and the positive staining of annexin V in EEC. These findings suggest that IFN-gamma promotes implantation by stimulating EEC to produce CXCL11, which induces migration of trophoblast cells and T cells, proliferation of ESC, and apoptosis of EEC.