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孕酮诱导阻断因子(PIBF)介导孕酮诱导的蜕膜淋巴细胞细胞毒性抑制。

Progesterone induced blocking factor (PIBF) mediates progesterone induced suppression of decidual lymphocyte cytotoxicity.

作者信息

Laskarin Gordana, Tokmadzić Vlatka S, Strbo Natasa, Bogović Tatjana, Szekeres-Bartho Julia, Randić Ljiljana, Podack Eckhard R, Rukavina Daniel

机构信息

Department of Physiology and Immunology, Medical Faculty, University of Rijeka, Rijeka, Croatia.

出版信息

Am J Reprod Immunol. 2002 Oct;48(4):201-9. doi: 10.1034/j.1600-0897.2002.01133.x.

Abstract

PROBLEM

Progesterone induced blocking factor (PIBF) is a mediator of progesterone that blocks peripheral blood lytic natural killer (NK) activity. Progesterone or PIBF stimulated decidual macrophages block up-regulation of perforin expression in decidual lymphocytes (DL). Therefore, we investigated whether progesterone regulates cytotoxicity of DL. METHOD OD STUDY: Decidual mononuclear cells were cultured with progesterone. PIBF, progesterone and anti-PIBF antibody or in the medium only. Cytolytic activity of non-adherent DL was measured by PKH-26 (red) 2 hr cytolytic assay and flow cytometry. Perforin positive DL were detected by immunofluorescency and PIBF-positive cells by immunohistology.

RESULTS

Progesterone and PIBF, in a dose-dependent manner decreased cytotoxicity of DL against K-562 targets, and perforin egzocytosys was blocked. Anti-PIBF antibodies reversed the progesterone mediated reduction in cytolytic activity of DL. PIBF positive cells were found in first trimester pregnancy decidua.

CONCLUSION

The results indicate possible role for PIBF, as a mediator of progesterone in regulation of DL cytolytic activity at the maternal-foetal (M-F) interface.

摘要

问题

孕酮诱导阻断因子(PIBF)是孕酮的一种介质,可阻断外周血溶细胞性自然杀伤(NK)活性。孕酮或PIBF刺激的蜕膜巨噬细胞可阻断蜕膜淋巴细胞(DL)中穿孔素表达的上调。因此,我们研究了孕酮是否调节DL的细胞毒性。

方法

将蜕膜单核细胞与孕酮、PIBF、孕酮和抗PIBF抗体一起培养,或仅在培养基中培养。通过PKH-26(红色)2小时细胞毒性试验和流式细胞术测量非贴壁DL的溶细胞活性。通过免疫荧光检测穿孔素阳性DL,通过免疫组织学检测PIBF阳性细胞。

结果

孕酮和PIBF以剂量依赖方式降低DL对K-562靶标的细胞毒性,并阻断穿孔素胞吐作用。抗PIBF抗体逆转了孕酮介导的DL溶细胞活性降低。在孕早期蜕膜中发现了PIBF阳性细胞。

结论

结果表明PIBF作为孕酮的介质在调节母胎(M-F)界面DL溶细胞活性中可能发挥作用。

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