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激活素A誘導(dǎo)小鼠單核巨噬細(xì)胞分化和成熟的作用研究

發(fā)布時間:2018-03-03 12:09

  本文選題:激活素A 切入點(diǎn):單核細(xì)胞 出處:《吉林大學(xué)》2010年碩士論文 論文類型:學(xué)位論文


【摘要】: 激活素A(Activin A)屬于轉(zhuǎn)化生長因子-β(TGF-β)超家族成員,我們前期研究顯示,激活素A具有誘導(dǎo)小鼠腹腔巨噬細(xì)胞活化及誘導(dǎo)巨噬細(xì)胞系RAW264.7細(xì)胞向樹突狀細(xì)胞(DC)分化作用,推測激活素A對外周血單核細(xì)胞及組織中成熟巨噬細(xì)胞的作用可能存在差異。因此,本研究通過體外培養(yǎng)小鼠外周血單核細(xì)胞及腹腔巨噬細(xì)胞,進(jìn)一步探討激活素A誘導(dǎo)單核巨噬細(xì)胞分化和成熟的作用。 研究結(jié)果顯示,激活素A刺激體外培養(yǎng)小鼠外周血單核細(xì)胞后,瑞士-吉姆薩染色顯示細(xì)胞呈樹突樣細(xì)胞形態(tài)學(xué)特征變化,流式細(xì)胞術(shù)檢測發(fā)現(xiàn)細(xì)胞表面樹突狀細(xì)胞標(biāo)志CD11c及CD40表達(dá)增高,ELISA檢測表明IL-12分泌水平增加,提示激活素A可以誘導(dǎo)小鼠外周血單核細(xì)胞向樹突狀細(xì)胞分化。激活素A作用于小鼠腹腔巨噬細(xì)胞,則促進(jìn)細(xì)胞表面CD68表達(dá),但對CD11c的表達(dá)無影響,同時促進(jìn)其分泌NO和IL-10,激活素A還能明顯上調(diào)Ⅱ型巨噬細(xì)胞(M2)標(biāo)志物精氨酸酶1(Arginase 1)的表達(dá),提示激活素A可以促進(jìn)小鼠腹腔巨噬細(xì)胞向Ⅱ型巨噬細(xì)胞分化成熟,但不能誘導(dǎo)小鼠腹腔巨噬細(xì)胞向DC分化。 上述資料表明,激活素A的作用與單核巨噬細(xì)胞分化成熟的狀態(tài)有關(guān),作用于小鼠外周血中未成熟的單核細(xì)胞可誘導(dǎo)其向DC分化;而作用于成熟的小鼠腹腔巨噬細(xì)胞,則促進(jìn)其向M2型分化成熟;因此,激活素A即可參與機(jī)體天然免疫應(yīng)答也可參與獲得性免疫應(yīng)答的調(diào)節(jié)。
[Abstract]:Activin A (Activin A) is a member of the transforming growth factor- 尾 (TGF- 尾) superfamily. Our previous studies have shown that activin A can induce the activation of murine peritoneal macrophages and induce the differentiation of macrophages from RAW264.7 cells to dendritic cells. It is speculated that the effect of activin A on peripheral blood monocytes and mature macrophages may be different. Therefore, in this study, mouse peripheral blood monocytes and peritoneal macrophages were cultured in vitro. To further investigate the role of activin A in the differentiation and maturation of mononuclear macrophages. The results showed that after stimulation of mouse peripheral blood monocytes by activin A in vitro, Switzerland-Gimsa staining showed that the cells showed dendritic cell morphological changes. Flow cytometry showed that the expression of CD11c and CD40 in dendritic cells was increased. Elisa showed that the level of IL-12 secretion was increased. It was suggested that activin A could induce the differentiation of peripheral blood monocytes into dendritic cells, but activin A could promote the expression of CD68 on the surface of peritoneal macrophages, but had no effect on the expression of CD11c. At the same time, the secretion of no and IL-10 was enhanced by activin A, and the expression of arginase 1 (Arginase 1), the marker of type 鈪,

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