复发性阿弗他溃疡患者血清中IL-17和IL-23的表达-论文.pdf

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1、第39卷第1期贵阳医学院学报VO1．39NO．12014年2月JOURNAL0FGUIYANGMEDICALCOLLEGE2014．2·论著·复发性阿弗他溃疡患者血清中IL一17和IL一23的表达水彭于治，蔡扬(1．贵阳医学院附院口腔内科，贵州贵阳550004；2．贵阳中医学院第一附院口腔科，贵州贵阳550001)[摘要]目的：探讨IL．17及IL-23在复发性阿弗他溃疡(RAU)患者血清中的表达及意义。方法：RAU患者40例(其中轻型3O例，重型10例)及健康对照20例，分析其免疫功能状态，采用ELISA法检测其溃疡发作

2、期外周血血清中IL一17、IL-23蛋白表达水平，分析二者的相关性。结果：(1)RAU患者CIM、CIM／8、CD16+56低于对照组；IgM、CH50高于对照组，而c3低于对照组，差异有统计学意义(P<0．05)；(2)RAU患者发作期外周血中IL一17及IL-23蛋白表达水平高于对照组，差异有统计学意义(P<0．01)，但在轻型及重型RAU间差异无统计学意义(P>0．05)，IL一17与IL一23表达水平间不存在相关性(r=一0．038，P>0．05)。结论：RAU患者存在细胞免疫功能降低和体液免疫功能紊乱的症状，RA

3、U患者溃疡发作期外周血中IL一17及IL-23蛋白表达增高，这可能在RAU患者溃疡发生中起一定作用。[关键词]口腔溃疡；免疫，细胞；白细胞介素17；白细胞介素23[中图分类号]R781．5[文献标识码]A[文章编号]1000-2707(2014)01-0018-03TheExpressionofInterleukin一17andInterleukin-23ProteinsinPeripheralbloodofPatientswithRecurrentAphthousUlcerPENGYuzhi，CAIYang(J．Depa

4、rtmentofStomatology，theAffiliatedHospitalofGu咖ngMedwalCollege，Gu咖ng550004，Guizhou，China；2．DepartmentofStomatology，theFirstAffiliatedHospitalofGuiyangTraditionalChineseMedicineCollege，Gu】ng550004，Gu~hou，China)[Abstract]Objective：ToinvestigatetheexpressionsofIL一17an

5、dIL-23proteinsintheserumofpa—tientswithrecurrentapht11OUSulcers(RAU)andelucidatethepossibleroleofIL．17andIL．23inthepathogenesisofRAU．Methods：40patientswithRAU(30casesofminoraphthousulcernamedMi．AUand10casesofmajoraphthousulcernamedniAU、wereenrolledinresearchgroupa

6、nd20healthypeopleservedascontro1．TheexpressionsofIL．17andIL-23proteinsinperipheralbloodwereinvestigatedbyusingELISAandtheirclinicalsignificanceinRAUwasanalyzedbySPSS11．5．Re．suits：TheCD4，CD4／CD8，CD16+56andC3levelsinpatientswithRAUweresignificantlylowerthanthoseinhe

7、althycontrol，andIgMandCH50levelsinpatientswithRAUweresignificantlyhigherthanthoseinhealthycontrol(P<0．05)：ThelevelsofIL．17andIL-23proteinsintheserumofpa—tientswithRAUweresignificantlyhigherthanthoseinhealthycontrol(P<0．O1)，whiletherewasnosignificantdiferencebetwee

8、nMiAUandMiAU(P>0．05)．Conclusions：Thereareimmunedysfunc—tionsinpatientswithRAU．IL-17andIL-23up—regulatingmayplaysomeroleintheimmunepatho-genesisofmU．[Key