简介：Clusterinisa75-80kDaheterodimericglycoprotein,thatisproducedinmosttissuesbutwhichexactbiologicalroleisstillnotclear.Particularly,itsroleinprotectionorpromotionofapoptosisisheavilydisputed,sincedatasupportingbothviewshavebeenreportedinseveralindependentstudies.Toclarifythisissue,andalsotodeterminewhetherclusterinexpressionitselfmightbeaffectedbyapoptosis,inthepresentstudy,ratthymocytesweretreatedwithdexamethasone,-asyntheticglucocorticoidthatelicitsapoptosisinthymocytes-,andclusterinmRNAexpressionwasanalyzedbysemi-quantitativeRT-PCRbeforeandafterinductionofapoptosis.Interestingly,neitherthetreatmentwithdexamethasoneinvitronortriggeringofapoptosisinvivoup-regulatedclusterinexpression,opposingtheviewthatclusterinisinvolvedinapoptoticprocesses.Ontheotherhand,anewclusterinmRNAisoformwasdetectedandisolated,whoseexpressionwasrestrictedtofreshlyisolatedthymocytes.Thisnovelisoformlacksthepost-translationalproteolyticcleavagesiteandisthereforepredictedtoencodeamonomericprotein.Thebiologicalfunctionundernormalcircumstances,however,willneedfurtherinvestigationsforclarification.Whileapoptosiscouldnotmodulateclusterinexpression,activationofthymocyteswithconcanavalinAandinterleukin-2resultedinup-regulationofclusterinmRNAlevel,indicatingthatclusterinexpressionisratherunderthecontrolofcellactivation-mediatedratherthanapoptosis-inducedsignals.

简介：自我忍耐的损失和汽车反应的淋巴细胞的扩大是汽车免疫的基础。当保证的协调过程与非病理学的结果调整了细胞质和压力反应，Apoptosis和由吞噬细胞的apoptotic房间的快速的清理通常发生。在apoptotic房间的清理的缺点将贡献自我反应的淋巴细胞的产生，它驾驶象风湿性关节炎(RA)和全身的豺狼座erythematosus(SLE)那样的自体免疫的混乱。cytokines(IL-12，IL-23，和IL-27)和IL-10的IL-12家庭被吞噬细胞的巨噬细胞生产并且在对病原体的有免疫力的回答期间在介绍抗原的房间(APC)和受动器淋巴细胞的规定起关键作用。这些cytokines和他们的dysregulated活动的不恰当的表示强烈在几自体免疫的疾病的致病被含有。由吞噬细胞的APC的支持inflammatory和反煽动性的cytokines的生产精巧地作为内在的机制的部分在apoptotic房间的摄取期间被调整阻止煽动性的自体免疫的反应。怎么导出房间的信号调整的apoptoticcytokine生产糟糕被理解。由我们的组的最近的研究证明由激活的巨噬细胞的apoptotic房间的那个吞噬作用由激活一个新奇抄写抑压者导致IL-12p35基因表示的强壮的抑制，我们把它称为GC有约束力的蛋白质(GC-BP)，通过酷氨酸dephosphorylation。我们开始也正在理解位于apoptotic下面的分子的机制由吞噬细胞的IL-10的被触发房间的生产。阐明的这些研究愿望帮助一些新奇有免疫力的规章的机制并且与潜力探索对汽车抗原的有免疫力的回答的规定为自体免疫的混乱的处理发现新治疗学的目标。

简介：Anuranmetamorphosisinvolvessystematictransformationsofindividualorgansinathyroidhormone(TH)-dependentmanner.Morphologicalandcellularstudieshaveshownthattheremovaloflarvalorgans/tissuessuchthetailandthetadpoleintestinalepitheliumisthroughprogrammedcelldeathorapoptosis.RecentmolecularinvestigationssuggestthatTHregulatesmetamorphosisbyregulatingtargetgeneexpressionthroughthyroidhormonereceptors(TRs),whichareDNA-bindingtranscriptionfactors.CloningandcharacterizationofTHresponsegenesshowthatdiversegroupsofearlyresponsegenesareinducedbyTH.TheproductsoftheseTHresponsegenesarebelievedtodirectlyorindirectlyaffecttheexpressionand/orfunctionsofcelldeathgenes,whichareconservedatbothsequenceandfunctionlevelsindifferentanimalspecies.Amajorchallengeforfutureresearchliesatdeterminingthesignalingpathwaysleadingtotheactivationofapoptoticprocessesandwhetherdifferentdeathgenesareinvolvedintheregulationofapoptosisindifferenttissues/organstoeffecttissue-specifictransformations.

简介：<正>Althoughapoptosishasbeenrecentlydocumentedtotransmitimmunosuppressivesignals,theirsignificanceinallogeneictransplantationhasnotbeenreported.Inthepresentstudy,weinvestigatedtheinfluenceofdonorapoptoticsplenocytesonallograftsurvivalinaSDtoWistarratcardiactransplantmodel.Donorsplenocyteswereisolatedandirradiatedwithultraviolet(UV)toinduceapoptosisinvitro.5x107apoptotic,necroticoruntreateddonorspleencellsweretransfusedpreoperativelyandcardiacallogeneictransplantation

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