摘要
在感染性疾病中,淋巴因子与免疫调节机制密切相关。为了解在人类免疫缺陷病毒(HIV)感染患者中淋巴因子对多种刺激原的动态变化反应情况,以便进一步弄清HIV感染的病理变化机制,我们采用定量逆转录聚合酶链反应的方法(RT-PCR),对经植物血凝素(PHA)、商陆致丝裂素(PWM)、念珠菌蛋白(candidin)、抗CD3单克隆抗体(Anti-CD3MAb)和重组白介素2(rIL2)刺激后的HIV感染者及对照组外周血单一核细胞(PBMC)中的白介素2(IL2)、γ干扰素(IFN-γ)、白介素10(IL10)、白介素6(IL6)、肿瘤坏死因子α(TNF-α)和IL2受体(IL2R)的动态变化进行了比较。在HIV感染组中,其IL2和IL2R基因表达水平明显低于对照组。IL2和IFN-γ均由T辅助细胞一型(TH1)克隆产生,然而在HIV感染患者中,IFN-γ的水平却明显增高。IL10基因表达情况视刺激原的不同而不同。经PHA、candidin、rIL2(1000U)刺激后,HIV感染组IL10mRNA表达水平明显高于对照组,但经rIL2(10U)和Anti-CD3MAb刺激后却低于对照组。HIV感染组TNF-α基因表达开?
Cytokineswerecloselyrelatedtothemajorimmunoregulatorymechanismininfectiousdisease.ThekineticsofcytokinegeneexpressionsincludingIL-2,IFN-γ,IL-10,IL-6,TNF-αandIL-2receptorinPBMCfromHIVseropositiveandseronegativesubjectswerecomparedbyquantitativere-versetranscriptionpolymerasechainreactionstudiesstimulatedbyphytohaemaglutinin(PHA),poke-wedmitogen(PWM),candidin,anti-CD3monoclonalantibody(Anti-CD3mAb)andrecombinantIL-2(rIL-2).IL-2andIL-2receptor(IL-2R)toPHA,PWM,candidin,anti-CD3mAbandrIL-2stimulationweremarkedlyloweredinpatientswithHIVinfection.ItisknownthatTh1cloneproducesIL-2andIFN-γ,however,highlevelofINF-γgeneexpressionwasfoundinthePBMCofpatientswithHIVin-fectionstimulatedbyPHA,candidin,PWM,10unitsofrIL-2andanti-CD3mAb.IL-10geneexpressionpaternsdiferedfromstimulitostimuli,highlevelofgeneexpresionwasobservedintheHIVinfectiongroupstimulatedbyPHA,candidinandrIL-2(1000U),andlowlevelofexpresionstimulatedbyrIL-2(10U)andanti-CD3MAb.TNF-αgeneexpressioninHIVseropositivesubjectsstartedearlierandwithhigherlevel.IFN-γ,IL-10,IL-6andTNF-αgeneexpresionsinHIVseropositivesubjectsstimulatedbyIL-2were'dose-dependent',lowdose(10U)showedhighlevelsofIFN-γ,TNF-αandIL-6,lowIL-10,buthighdose(1000U)showedoppositeresultsascomparedwithHIVseronegativesubjects.IFN-γandIL-10geneex-pressionstimulatedbyrIL-2(10U),rIL-2(1000U),andanti-CD3mAbshowedreversedpatternsinbothHIVseropos-itiveandnegativesubjects,itindicatesthatthereisanendogenousregulationbetweenTh1andTh2cytokines.
出处
《中华皮肤科杂志》
CAS
CSCD
北大核心
1996年第3期157-160,共4页
Chinese Journal of Dermatology