中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
Chinese Journal of Pancreatology
2015年
5期
331-335
,共5页
蒋永剑%刘少军%张力胤%杨峰%何航%金忱%傅德良
蔣永劍%劉少軍%張力胤%楊峰%何航%金忱%傅德良
장영검%류소군%장력윤%양봉%하항%금침%부덕량
胰腺肿瘤%调节性T细胞%FOXP3%趋化因子
胰腺腫瘤%調節性T細胞%FOXP3%趨化因子
이선종류%조절성T세포%FOXP3%추화인자
Pancreatic neoplasms%Regulatory T cell%FOXP3%Chemokime
目的 明确介导调节性T( Treg)细胞在胰腺癌中聚集的主要趋化因子-趋化因子受体通路. 方法 应用酶联免疫吸附法( ELISA)测定人及小鼠胰腺癌组织和相应癌旁正常胰腺组织中FOXP3蛋白及趋化因子CCL2、CCL3、CCL5、CCL17、CXCL8水平;应用免疫荧光染色法检测人及小鼠胰腺癌组织中CCL5受体( CCR5 )的表达. 结果 人胰腺癌组织、癌旁正常胰腺组织FOXP3蛋白水平分别为(487.5 ±534.1)、(162.6 ±42.0)pg/mg;小鼠分别为(84.6 ±54.1)、(14.4 ±7.6)pg/mg. 胰腺癌组织FOXP3水平均显著高于癌旁胰腺组织(P值均<0.01). 人胰腺癌组织、癌旁正常胰腺组织趋化因子CCL2水平分别为(76.9 ±37.5 )、(40.8 ±25.5) pg/mg;CCL3 分别为(38.0 ±22.6)、(21.3 ±16.5) pg/mg;CCL5为(390.2 ±158.5)、(59.1 ±22.8)pg/mg;CCL17为(7.2 ±2.0)、(4.1 ±2.4)pg/mg;CXCL8为(9.3 ±5.5)、(6.3 ±5.2)pg/mg. 其中胰腺癌CCL2、CCL5、CCL17水平均显著高于癌旁胰腺组织,差异有统计学意义( P值均<0 .05 ). 小鼠胰腺癌组织、癌旁正常胰腺组织CCL2 水平分别为( 77 .9 ± 30.5)、(43.6 ±16.6)pg/mg蛋白;CCL3为(27.4 ±18.2)、(14.0 ±4.5)pg/mg;CCL5为(302.2 ±55.8)、(64.5 ±30.3)pg/mg;CCL17为(4.4 ±1.4)、(2.2 ±1.0) pg/mg;CXCL8为(55.1 ±55.1)、(93.4 ±7.3) pg/mg. 其中胰腺癌 CCL2、CCL5、CCL17 水平均显著高于癌旁胰腺组织,差异有统计学意义( P 值均<0 .05 ). 人及小鼠胰腺癌组织FOXP3水平与趋化因子差异值大的CCL5水平呈正相关. 免疫荧光染色也显示人及小鼠胰腺癌组织FOXP3 +细胞均有CCR5的表达. 结论 CCL5-CCR5通路是介导Treg细胞在胰腺癌组织中聚集的重要趋化因子-趋化因子受体通路.
目的 明確介導調節性T( Treg)細胞在胰腺癌中聚集的主要趨化因子-趨化因子受體通路. 方法 應用酶聯免疫吸附法( ELISA)測定人及小鼠胰腺癌組織和相應癌徬正常胰腺組織中FOXP3蛋白及趨化因子CCL2、CCL3、CCL5、CCL17、CXCL8水平;應用免疫熒光染色法檢測人及小鼠胰腺癌組織中CCL5受體( CCR5 )的錶達. 結果 人胰腺癌組織、癌徬正常胰腺組織FOXP3蛋白水平分彆為(487.5 ±534.1)、(162.6 ±42.0)pg/mg;小鼠分彆為(84.6 ±54.1)、(14.4 ±7.6)pg/mg. 胰腺癌組織FOXP3水平均顯著高于癌徬胰腺組織(P值均<0.01). 人胰腺癌組織、癌徬正常胰腺組織趨化因子CCL2水平分彆為(76.9 ±37.5 )、(40.8 ±25.5) pg/mg;CCL3 分彆為(38.0 ±22.6)、(21.3 ±16.5) pg/mg;CCL5為(390.2 ±158.5)、(59.1 ±22.8)pg/mg;CCL17為(7.2 ±2.0)、(4.1 ±2.4)pg/mg;CXCL8為(9.3 ±5.5)、(6.3 ±5.2)pg/mg. 其中胰腺癌CCL2、CCL5、CCL17水平均顯著高于癌徬胰腺組織,差異有統計學意義( P值均<0 .05 ). 小鼠胰腺癌組織、癌徬正常胰腺組織CCL2 水平分彆為( 77 .9 ± 30.5)、(43.6 ±16.6)pg/mg蛋白;CCL3為(27.4 ±18.2)、(14.0 ±4.5)pg/mg;CCL5為(302.2 ±55.8)、(64.5 ±30.3)pg/mg;CCL17為(4.4 ±1.4)、(2.2 ±1.0) pg/mg;CXCL8為(55.1 ±55.1)、(93.4 ±7.3) pg/mg. 其中胰腺癌 CCL2、CCL5、CCL17 水平均顯著高于癌徬胰腺組織,差異有統計學意義( P 值均<0 .05 ). 人及小鼠胰腺癌組織FOXP3水平與趨化因子差異值大的CCL5水平呈正相關. 免疫熒光染色也顯示人及小鼠胰腺癌組織FOXP3 +細胞均有CCR5的錶達. 結論 CCL5-CCR5通路是介導Treg細胞在胰腺癌組織中聚集的重要趨化因子-趨化因子受體通路.
목적 명학개도조절성T( Treg)세포재이선암중취집적주요추화인자-추화인자수체통로. 방법 응용매련면역흡부법( ELISA)측정인급소서이선암조직화상응암방정상이선조직중FOXP3단백급추화인자CCL2、CCL3、CCL5、CCL17、CXCL8수평;응용면역형광염색법검측인급소서이선암조직중CCL5수체( CCR5 )적표체. 결과 인이선암조직、암방정상이선조직FOXP3단백수평분별위(487.5 ±534.1)、(162.6 ±42.0)pg/mg;소서분별위(84.6 ±54.1)、(14.4 ±7.6)pg/mg. 이선암조직FOXP3수평균현저고우암방이선조직(P치균<0.01). 인이선암조직、암방정상이선조직추화인자CCL2수평분별위(76.9 ±37.5 )、(40.8 ±25.5) pg/mg;CCL3 분별위(38.0 ±22.6)、(21.3 ±16.5) pg/mg;CCL5위(390.2 ±158.5)、(59.1 ±22.8)pg/mg;CCL17위(7.2 ±2.0)、(4.1 ±2.4)pg/mg;CXCL8위(9.3 ±5.5)、(6.3 ±5.2)pg/mg. 기중이선암CCL2、CCL5、CCL17수평균현저고우암방이선조직,차이유통계학의의( P치균<0 .05 ). 소서이선암조직、암방정상이선조직CCL2 수평분별위( 77 .9 ± 30.5)、(43.6 ±16.6)pg/mg단백;CCL3위(27.4 ±18.2)、(14.0 ±4.5)pg/mg;CCL5위(302.2 ±55.8)、(64.5 ±30.3)pg/mg;CCL17위(4.4 ±1.4)、(2.2 ±1.0) pg/mg;CXCL8위(55.1 ±55.1)、(93.4 ±7.3) pg/mg. 기중이선암 CCL2、CCL5、CCL17 수평균현저고우암방이선조직,차이유통계학의의( P 치균<0 .05 ). 인급소서이선암조직FOXP3수평여추화인자차이치대적CCL5수평정정상관. 면역형광염색야현시인급소서이선암조직FOXP3 +세포균유CCR5적표체. 결론 CCL5-CCR5통로시개도Treg세포재이선암조직중취집적중요추화인자-추화인자수체통로.
Objective To confirm the main pathway of chemokine-chemokine receptor which mediates the accumulation of regulatory T cell ( Treg) in pancreatic cancer .Methods The concentrations of protein of FOXP3 and chemokines of CCL2, CCL3, CCL5, CCL17, CXCL8 in human and mouse pancreatic cancer and adjacent normal pancreatic tissue were measured by the method of enzyme-linked immunosorbent assay (ELISA).The receptor of chemokine CCL5 (CCR5) in human and mouse pancreatic cancer were determined by the immunofluorescent stain .Results The concentration of FOXP 3 protein in human pancreatic cancer and adjacent normal pancreatic tissue as (487.5 ±534.1) and (162.6 ±42.0) pg/mg, respectively, while they were (84.6 ±54.1) and (14.4 ±7.6) pg/mg, respectively in mouse.The concentration of FOXP3 protein were significantly higher in pancreatic cancer than those in adjacent normal pancreatic tissue .The concentration of CCL2 in human pancreatic cancer and adjacent normal pancreatic tissue as (76.9 ±37.5), (40.8 ±25.5) pg/mg, and the concentration of CCL3 as (38.0 ±22.6), (21.3 ±16.5) pg/mg, and the concentration of CCL5 were (390.2 ±158.5), (59.1 ±22.8) pg/mg, and the concentration of CCL17 as (7.2 ±2.0), (4.1 ±2.4)pg/mg, and the concentration of CXCL8 as (9.3 ±5.5), (6.3 ±5.2)pg/mg.The concentration of CCL2, CCL5, CCL17 in pancreatic cancer was significantly higher than those in adjacent normal pancreatic tissue (P<0.05).The concentration of CCL2 in mouse pancreatic cancer and adjacent normal pancreatic tissue as (77.9 ±30.5), (43.6 ±16.6) pg/mg, and the concentration of CCL3 was (27.4 ±18.2), (14.0 ±4.5)pg/mg, and the concentration of CCL5 was (302.2 ±55.8), (64.5 ±30.3) pg/mg; and the concentration of CCL17 was (4.4 ±1.4), (2.2 ±1.0)pg/mg;and the concentration of CXCL8 was (55.1 ± 55.1), ( 93.4 ±7.3 ) pg/mg.The concentration of CCL2, CCL5, CCL17 in pancreatic cancer were significantly higher than those in adjacent normal pancreatic tissue , and the difference between the two groups was statistically significant (P<0.05).The level of FOXP3 in pancreatic cancer was positively correlated with the concentration of chemokine CCL 5 both in human and mouse pancreatic cancer .Immunofluorescent staining indicated that the FOXP3 +cells also expressed CCR5.Conclusions The CCL5-CCR5 is the main chemokine-chemokine receptor pathway mediating the accumulation of Treg cells in pancreatic cancer .
