jak2stat3途径在il-6抑制lps诱导的树突状细胞分化成熟中的作用

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1、JAK2/STAT3途径在IL-6抑制LPS诱导的树突状细胞分化成熟中的作用赵永亮，余佩武，雷晓，刘伟，饶芸（第三军医大学西南医院全军普外科中心，微创胃肠外科中心，重庆400038）摘要：目的观察JAK2/STAT3信号途径在IL-6抑制LPS诱导的小鼠髓源性DC（BMDC）分化成熟中的作用。方法分离小鼠骨髓细胞，采用黏附法结合GM-CSF和IL-4刺激法在体外培养髓源性DCs（BMDCs）；用相差倒置显微镜观察BMDCs的形态特点；用LPS诱导DC成熟；采用流式细胞术观察IL-6处理与否，LPS诱导的BMDCs在表型上的变化；Westernblot检测BMDC细胞

2、质p-JAK2、总STAT3和p-STAT3的表达水平。结果形态观察和FCM分析的结果表明：体外成功培养了纯度较高的高表达CD11c的BMDCs，LPS能明显诱导BMDCs表面MHC-Ⅱ类分子和共刺激分子CD80、CD86、CD40的表达上调；而经过IL-6处理后，LPS诱导BMDCs表面MHC-Ⅱ类分子、CD80、CD86、CD40表达上调的能力被显著削弱(P<0.01)。Westernblot结果显示，与单独用LPS处理的BMDCs相比，经IL-6处理后的BMDC中p-JAK2、p-STAT3表达随作用时间增加而明显上调，提示IL-6促进JAK2/STAT3信号

3、途径活化。结论JAK2/STAT3信号途径参与了IL-6抑制LPS诱导的BMDC成熟过程。关键词：髓源性树突状细胞；IL-6；LPS；JAK2/STAT3信号途径中图法分类号：文献标识码：AIL-6suppressesLPS-inducedDCmaturationviaJAK2/STAT3pathwayZHAOYong-liang,YUPei-wu,LEIXiao,LIUWei,RAOYun(DepartmentofGeneralSurgery,SouthwestHospital,ThirdMilitaryMedicalUniversity,Chongqing400

4、038,China)Abstract:　ObjectiveToinvestigatetheroleofJAK2/STAT3signalingpathwayinIL-6-inducedsuppressiononthematurationofmousebonemarrow-deriveddendriticcells(BMDCs)afterLPStreatment.MethodsToobtainimmatureBMDCs,mousebonemarrowcellswereisolatedandculturedincompleteculturemediumcontaining

5、GM-CSFandIL-4afterremovingthenonadherentcells.Thecellmorphologywasobservedbyusingaphasecontrastinvertedmicroscope.LPSwasaddedintotheculturemediumofBMDCstoinducethecellmaturation.TheexpressionofcostimulatorsandMHCclassIImoleculesonthesurfaceofLPS-treatedBMDCswithorwithoutIL-6treatmentwa

6、sanalyzedbyflowcytometry.Theexpressionofp-JAK2,STAT3andp-STAT3weredetectedbyWesternblotanalysis.ResultsDCswereobtainedfrommousebonemarrowwithnormalmorphologyandhighpurity.ComparedwithBMDCsincubatedwithLPSonly,LPS-treatedDCsculturedinthepresenceofIL-6expressedmuchlowerlevelsofCD40,CD80,

7、CD86andMHCclassIImolecules.Theexpressionlevelofcytoplasmicp-JAK2andp-STAT3inBMDCstreatedwithbothLPSandIL-6weremuchhigherthaninBMDCstreatedwithLPSonly.ConclusionJAK2/STAT3pathwaymaybeinvolvedinthesuppressionofLPS-inducedDCsmaturationbyIL-6.Keywords:bonemarrowderiveddendriticcells;IL-6