【摘要】：目的探討HBe Ag對LPS誘導小鼠骨髓源性樹突狀細胞(DC)成熟的影響。方法體外誘導C57BL/6小鼠骨髓細胞分化成未成熟樹突狀細胞,經CD11c磁珠分選純化后將DCs隨機分為空白對照組、LPS刺激組、HBe Ag+LPS刺激組。流式檢測DC表型變化,混合淋巴反應(MLR)檢測DC促T淋巴細胞增殖能力,酶聯(lián)免疫法(ELISA)檢測細胞上清液中IL-12的分泌水平,Western blot檢測p38磷酸化水平,并設置SB203580組為陽性對照探討細胞IL-12分泌的可能調節(jié)機制。結果 LPS刺激未成熟DC引起細胞表面MHC-Ⅱ、CD86表達升高,刺激同種異體淋巴細胞增殖能力增強,IL-12分泌量增高。HBe Ag可抑制LPS促進DC表面MHC-Ⅱ、CD86表達升高和促淋巴細胞增殖能力增強的作用。LPS刺激DC可引起p38磷酸化水平升高,并呈時間依賴性;HBe Ag或SB203580預處理細胞再予LPS刺激,磷酸化p38表達和IL-12分泌較單純LPS刺激組明顯下降。結論 HBe Ag對LPS引起的樹突狀細胞的成熟有一定的抑制作用,且HBe Ag可能通過抑制p38MAPK信號通路下調LPS誘導的樹突狀細胞IL-12的產生。
[Abstract]:Objective to investigate the effect of HBe Ag on (DC) maturation of mouse bone marrow derived dendritic cells induced by LPS. Methods Bone marrow cells of C57BL/6 mice were induced to differentiate into immature dendritic cells in vitro. DCs was randomly divided into blank control group and, HBe Ag LPS stimulation group after DCs was purified by CD11c magnetic beads. The phenotypic changes of DC were detected by flow cytometry, the proliferation ability of T lymphocytes stimulated by DC was detected by mixed lymphoid reaction (MLR), the level of IL-12 secretion in supernatant was detected by enzyme linked immunosorbent assay (ELISA), and the phosphorylation level of p38 was detected by, Western blot. The possible regulation mechanism of IL-12 secretion in SB203580 group was discussed. Results LPS stimulated immature DC increased the expression of MHC- 鈪，

本文編號：2422035