简介：全部的联合代替是为有停用关节炎和联合机能障碍的病人的治疗的一个高度成功的外科的过程。随着时间的过去，与活动的高水平和关节的用法，然而植入穿粒子从明白表示的表面被产生。这些穿粒子能在implant(periprostheticosteolysis)附近导致煽动性的反应，和随后的骨头再吞的激活。单核白血球/巨噬细胞系的房间安排这长期的煽动性的回答，它被支持inflammatory(M1)统治巨噬细胞显型而非一反煽动性的支持织物的愈合(M2)巨噬细胞显型。当它被显示出时，那interleukin-4(IL-4)有选择地极化向支持骨头愈合的M2反煽动性的显型的巨噬细胞，而非发炎，很少对这在通过IL-4的极化在哪个是很有效的在发生或调节的时间功课被知道。这个工作的目标是与polymethylmethacrylate(PMMA)的联合响应挑战学习鼠科的巨噬细胞极化和cytokine版本的时间功课粒子，lipopolysaccharide(LPS)和在vitro的IL-4。有IL-4的质问粒子的单核白血球/巨噬细胞的处理导致了支持inflammatorycytokines和可诱导的氮的氧化物synthase(iNOS)的起始的抑制生产和随后的极化进M2反煽动性的显型。当IL-4在PMMA粒子挑战前被交付时，这结果被优化，到M1显型而非到未遂(M0)巨噬细胞。这极化的效果在一堂5天的时间功课上被支撑。进M2显型的M1巨噬细胞的极化可以是策略减轻穿粒子联系periprostheticosteolysis。

简介：Toinvestigatetheeffectsofantisenseoligonucleotidesontheexpressionofmacrophagemigrationinhibitoryfactor(MIF)onmacrophages,themousephosphorothioateoligonucleotidesweredesignedandsynthesizedwiththesequencesofantisense,5'-TACGGATACAAGTAGCAC-3'；Sense,5'-ATGC-CTATGTTCATCGTG-3'；Missense,5'-CTCTCAGACTCGATCTGT-3'.Thesephosphorothioateoligonucleotideswerethentransfectedintoculturedmacrophages(RAW264.7)byluciferasevector,andthetransfectedmacrophageswereincubatedwithLipopolysaccharide(LPS)(1ng/ml)forvariousperiodsoftimesandcollectedafterwards.ThecontentofMIFproteinintheculturalsupernatantswasdeterminedbyELISA,cellularRNAextractedandtheexpressionofMIFmRNAwasexaminedbyRT-PCRanalysis.TheexperimentalresultsshowedthatLPScouldinduceatime-dependentspecificexpressionofMIFonmacrophages,inwhichtheMIFmRNAincellsandtheMIFproteininculturalsupernatantsappearedafter3handreachedtheirhighestconcentrationat9-12hafterLPSstimulation.ThelevelsofmRNAandproteinsinthemacrophagestreatedwithantisenseolignucleotidesweredecreasedsignificantlyafterstimulationwithLPSincomparisonwiththatofstimulationwithLPSaloneorwiththatwithLPSplussenseormissenseoligonucleotides.TherewerenodifferencesamongthosewithoutLPSstimulation.ItisconcludedthatmacrophagesstimulatedwithLPSexpressMIF,andtheantisenseolignucleotidesofMIFinhibittheexpressionofMIFmRNAaswellasthesecretionofMIFproteinsinmacrophages.

简介：InteractionbetweencytotoxicTlymphocyte-associatedantigen-4(CTLA4,CD152)andB7molecules(B7-1andB7-2)isofimportanceinthecellulareventsoflymphocyte,includingantigen-specificT-cellactivationandinductionofautoreactiveT-cell.WedescribehaerethefirstintroductionofamurinesolubleCTLA4gene,CTLA4Ig,toMm1cells,amacrophagiccellline.CTLA4IgwassuccessfullyexpressedonMm1cellsandtheexpressedCTLA4IgwasfoundtobefunctionallyactiveintheirbindingtoB7moleculesbyflowcytometryandimmunofluorescencestudies.ThebiologicalactivityofCTLA4IgfromthetransfectedMm1cellswasstudiedandshowedinhibitoryactivityonmixedlymphocyteculture.AhighCTLA4Igproducingmacrophagiccelllinewasobtained.AsMm1cellswereregardedasdifficultforgenetransfectionandtherehassofarbeennoreportonexpressionofCTLA4IggeneonMm1cells,theseresultssuggestedthattheCELA4IgexpressingMm1cellscouldbeusefulforanalysisofCTLA4andB8moleculeinteractioninbothmacrophageandT-cell.

简介：巨噬细胞经由secreting支持inflammatory调停人，phagocytosing微生物和介绍抗原在天生的有免疫力、获得的免疫者起关键作用。ActivinA，转变生长因素(TGF-)总科的一个成员，被巨噬细胞和microglia细胞生产。在这研究，我们在老鼠巨噬细胞房间线RAW264.7房间上作为一个支持inflammatory因素报导了activinA的直接效果。我们的数据表明activinA不能仅仅从RAW264.7房间增加IL-1和IL-6生产，而且支持pinocytic和RAW264.7房间的吞噬细胞的活动。另外，activinARAW264.7房间的表面上的显然起来调整的MHCII表示，而没影响MHC我表示。ActivinA也提高了CD80表示，它是激活的巨噬细胞的一个标记，但是没影响RAW264.7房间增长。这些数据建议activinA可以经由支持休息巨噬细胞的激活调整主要调停巨噬细胞的天生、获得的有免疫力的反应。

简介：M-CSF是在由导致MAPK激活的巨噬细胞开发的关键cytokine，并且营地能禁止煽动性的刺激导致的MAPK激活。在M-CSF-inducedMAPK激活上并且在巨噬细胞开发探索营地的效果，骨头的模型导出髓的鼠科的巨噬细胞(BMM)被使用。M-CSF-inducedMAPK激活上的营地的效果被营地的西方的弄污的试金，和效果在CD14上分析，F4/80表示被FACS分析在巨噬细胞开发期间检验。巨噬细胞形态学显示出巨噬细胞开发的模型的成功的建立。西方的弄污试金表明M-CSF在成熟、不成熟的巨噬细胞激活英皇家空军之阶级最低之兵，JNK和p38，并且营地以一种时间依赖者方式禁止了M-CSF-induced英皇家空军之阶级最低之兵，JNK和p38激活。FACS分析表明巨噬细胞开发与营地预告的处理被损害。在结论，营地由压制M-CSF-inducedMAPK激活调制巨噬细胞开发。

简介：

简介：MIF受体的最近的克隆在我们分子的生物学的理解和MIF的免疫学充满重要差距。MIF受体象MIF一样，不掉进蛋白质调停人的任何确定的家庭，提供为MIF信号transduction的结构、功能的分析的新挑战和机会。

简介：无

简介：Objective:ToexploretheeffectsofnuclearM-CSFontheprocessoftumorigenesis.Methods:FunctionalpartofM-CSFcDNAwasinsertedintoaneukaryoticexpressionplasmidpCMV/myc/nuc,whichcanaddthreeNLStotheC-terminaloftheexpressedproteinanddirecttheproteinintothecellnuclei.TheconstructedplasmidwastransferredintoNIH3T3cellsandthecellcloneswereselectedbyG-418selection.CellclonesstableexpressingtargetproteinwereidentifiedbyRT-PCR,ABCimmunohistochemistryassayandWesternblot.Cellgrowthkineticsanalysesthroughgrowthcurves,celldoublingtime,MTTtestandanti-senseoligodeoxynucleotide(ASODN)inhibitingcellgrowthtestwereperformedtoidentifycellsproliferationpotential.Results:Thetransfectedcellsshowedelevatedproliferationpotentialoverthecontrolcells.Conclusion:AbnormalappearanceofM-CSFinnucleuscouldenhancecellproliferation,whichsuggeststhatcytokineisoformswithincellnucleusmightplaytranscriptionfactor-likerole.

简介：AIMMacrophagemigrationinhibitoryfactor(MIF)isapro-inflammatorycytokineinvolvedinthepathogenesisofavarietyofautoimmuneandinflammatorydiseases,includingarthritis,glomerulonephritis,Gram-positiveandGram-negativesepsis,andatherogenesis.RecentstudiesshowedthatCD74(antigen-associatedinvariantchainⅡ)isahigh-affinitymembrane-bindingproteinforMIF.ThepurposeofthepresentstudywastoexpresstherecombinanthumanCD74inE.coliandinhibittheactivityofMIFbyusingrecombinantCD74invitro.

简介：

简介：客观：为了与M-CSFR验证MAF-J6-1受体的抗原协会并且进一步学习M-CSF和它的受体的角色，调停了在支持白血病的房间增长的juxtacrine。方法：MAF-J6-1RRE2的Monoclonal抗体(McAb)和rhM-CSFR的polyclonal抗体(PolyAb)被准备。到M-CSFR的McAbRE2的特性被ELISA被间接ELISA，有J6-1房间殖民地形成的跨neutralizing试金和中立化测试证实。结果：到M-CSFR的净化的RE2的反应活动是超过1：16000。M-CSFR和MAF-J6-1R的禁止的活动能被RE2和anti-M-CSFR抗体堵住。到M-CSFR的RE2的反应能被M-CSFR减少。结论：到M-CSFR的RE2的特性被证实，有M-CSFR的MAF-J6-1R的抗原协会被证明。它建议M-CSF和它的受体调停了auto-juxtacrine刺激能是在白血病或nonhematological恶意的起作用的机制。

简介：AbstractBackground:Macrophages are involved in the pathogenesis of idiopathic pulmonary fibrosis, partially by activating lung fibroblasts. However, how macrophages communicate with lung fibroblasts is largely unexplored. Exosomes can mediate intercellular communication, whereas its role in lung fibrogenesis is unclear. Here we aim to investigate whether exosomes can mediate the crosstalk between macrophages and lung fibroblasts and subsequently induce fibrosis.Methods:In vivo, bleomycin (BLM)-induced lung fibrosis model was established and macrophages infiltration was examined. The effects of GW4869, an exosomes inhibitor, on lung fibrosis were assessed. Moreover, macrophage exosomes were injected into mice to observe its pro-fibrotic effects. In vitro, exosomes derived from angiotensin II (Ang II)-stimulated macrophages were collected. Then, lung fibroblasts were treated with the exosomes. Twenty-four hours later, protein levels of α-collagen I, angiotensin II type 1 receptor (AT1R), transforming growth factor-β (TGF-β), and phospho-Smad2/3 (p-Smad2/3) in lung fibroblasts were examined. The Student’s t test or analysis of variance were used for statistical analysis.Results:In vivo, BLM-treated mice showed enhanced infiltration of macrophages, increased fibrotic alterations, and higher levels of Ang II and AT1R. GW4869 attenuated BLM-induced pulmonary fibrosis. Mice with exosomes injection showed fibrotic features with higher levels of Ang II and AT1R, which was reversed by irbesartan. In vitro, we found that macrophages secreted a great number of exosomes. The exosomes were taken by fibroblasts and resulted in higher levels of AT1R (0.22 ± 0.02 vs. 0.07 ± 0.02, t = 8.66, P = 0.001), TGF-β (0.54 ± 0.05 vs. 0.09 ± 0.06, t= 10.00, P < 0.001), p-Smad2/3 (0.58 ± 0.06 vs. 0.07 ± 0.03, t= 12.86, P < 0.001) and α-collagen I (0.27 ± 0.02 vs. 0.16 ± 0.01, t = 7.01, P = 0.002), and increased Ang II secretion (62.27 ± 7.32 vs. 9.56 ± 1.68, t= 12.16, P < 0.001). Interestingly, Ang II increased the number of macrophage exosomes, and the protein levels of Alix (1.45 ± 0.15 vs. 1.00 ± 0.10, t = 4.32, P = 0.012), AT1R (4.05 ± 0.64 vs. 1.00 ± 0.09, t = 8.17, P = 0.001), and glyceraldehyde-3-phosphate dehydrogenase (2.13 ± 0.36 vs. 1.00 ± 0.10, t = 5.28, P = 0.006) were increased in exosomes secreted by the same number of macrophages, indicating a positive loop between Ang II and exosomes production.Conclusions:Exosomes mediate intercellular communication between macrophages and fibroblasts plays an important role in BLM-induced pulmonary fibrosis.

简介：

简介：

简介：Granulocyte巨噬细胞刺激殖民地的因素(GM-CSF)是一个重要造血的生长因素和有免疫力的调节的人。GM-CSF也在各种各样的传播白血球的功能的活动有深刻效果。它被许多房间类型在收到有免疫力的刺激之上包括T房间，巨噬细胞，endothelial房间和成纤维细胞生产。尽管GM-CSF局部地被生产，它能以一种paracrine方式行动到在主人防卫提高他们的功能的成员传播neutrophils，单核白血球和淋巴细胞。最近的集中的调查为它增加树枝状的房间(DC)成熟和功能以及巨噬细胞活动的能力作为一个有免疫力的助手在GM-CSF的应用程序上被集中。在经历化疗的癌症病人对待嗜中性白血球减少症临床上被使用，在在治疗期间的爱滋病病人，并且在在骨髓移植以后的病人。有趣地，GM-CSF-deficient老鼠的造血的系统看起来正常；最重要的变化在一些特定的T房间回答。尽管GM-CSF的分子的克隆用T房间的cDNA图书馆被执行，T房间在激活以后生产GM-CSF，是众所周知的，在T房间功能上有在由T房间和它的效果的生产的这cytokine的系统的调查的缺乏。在这篇文章，我们将在T房间主要集中于GM-CSF的免疫生物学。

简介：巨噬细胞(目的)的Apoptosis禁止者，人的Spα的一个相当或相同事物；，是一只老鼠scavenger受体的可溶的成员充满半胱氨酸的总科(SRCR-SF)。这个家庭集成没有统一功能还为被描述了的天生、适应的有免疫力的房间表示的一组蛋白质。多种的功能被归功于瞄准，从在在到在自体免疫的病理的类脂化合物新陈代谢和反煽动性的效果的thymic选择期间的淋巴细胞的生存能力支持。在现在的报告，目的病原体绑定性质被探索了。由使用在哺乳动物的细胞表示的目的(rAIM)的一种recombinant形式，这蛋白质能绑并且聚集克积极、克否定的细菌，以及病原、腐生的真菌的种类，这被显示出。重要地，浆液也绑在目的微生物和分泌物的从老鼠的内长的目的很快在跟随暴露到保存微生物引起的房间墙部件的老鼠怒气巨噬细胞被导致。老鼠splenocytes上的ligands也是的著名细菌、真菌的像使用费的受体(TLR)导致的Cytokine版本面对rAIM禁止了。而且，联系病原体的分子的模式(PAMP)的老鼠模型导致了腐败细菌、真菌的起源的吃惊证明浆液目的层次以一种时间依赖者方式变化了。总的来说，这些数据建议那个目的由在病原体侵略期间支持天生的体液的防卫起一个一般homeostatic作用。

简介：Amurinemacrophage-likecelllineJ774,acquired,inresponsetoLPS,anabilitytokilltumornecrosisfactor(TNF)-insensitivetargetP815mastocytomacellswhereasanothercellline,P388D1didnot,LPStriggeredsignalingmechanismsbetweenthetwocelllineswerecomparedwithanaimtoinquireaboutthepossiblenatureoftheabove-mentioneddifference,TheresultswhowedthattwocelllinesrespondtoLPS-treatmentbyparallelactivationofbothphospholipasesCandA2(PLCandPLA2)toapproximatelythesameextent.ThemaximumresponseoftothenzymesofJ774cellswasnotedwithin10minthetreatmentwhereasthatofP388D1cellsrequiredmorethan20min,TheotherpropertiesofLPS-responsiveenzymesstudiedweresimilarbetweentwocelllines,includingActivationofPLCandPLA2andPKCinmacrophagesbyLPS.Ca2+augmentationofenzymeactivation,participationofguaninenucleotidebinding(G)proteinsintheinitialactivationpreocesses,andinhibitionofenzymeactivationbythepriortreatmentofcellswithcholeraorpertussistoxinsetc.Moreover,LPS-triggeredactivationofPLCandPLA2wasfoundtobefollowedbytheincreaseofPKCactivitiesinbothcelllines.Inspiteofthesesimilarities.J774cellspossessedbothbasicandacidicformsofPKCactivities,whileP388D1cellsownedonlyPKCofbasicform,Nevertheless,thequestionwhyJ774cellsbutnotP388D1cells,canacquirethetumoricidalactivity,aganistP815,cellsfollowingLPStreatmentrematinstobeanswered.

简介：

简介：Amurinemacrophage-likecellline,J774,acquried,inresponsetoLPS,anabilitytokilltumornecrosisfactor（TNF）-insensitivetargetP815mastocytomacells,whereasanothercellline,P388D1,didnot.LPS-triggeredsignalingmechanismsbetweenthetwocelllineswerecomparedwithanaimtoinquireaboutthepossiblenatureoftheabove-mentioneddifference.TheresultsshowedthattwocelllinesrespondtoLPS-treatmentbyparallelactivationofbothphospholipasesCandA2（PLCandPLA2）toapproximatelythesameextent.ThemaximumresponseofbothenzymesofJ774cellswasnotedwithin10minofthetreatment,whereasthatofP388D1cellsrequiredmorethan20min.TheotherpropertiesofLPS-responsiveenzymesstudiedweresimilarbetweentwocelllines,ineludingActivationofPLCandPLA2andPKCinmacrophagesbyLPSCa2+augmentationofenzymeactivation,participationofguaninenucleotidebinding（G）proteinsintheinitialactivationprocesses,andinhibitionofenzymeactivationbythepriortreatmentofcellswithcholeraorpartussistoxinsetc.Moreover,LPS-triggeredactivationofPLCandPLA2wasfoundtobefollowedbytheincreaseofPKCactivitiesinbothcelllines.Inspiteofthesesimilarities,J774cellspossessedbothbasicandacidicformsofPKCactivities,whileP388D1cellsownedonlyPKCofbasicform.Nevertheless,thequestionwhyJ774cells,butnotP388D1cells,canacquirethetumoricidalactiyity,aganistP815cellsfollowingLPS-treatmentremainstobeanswered.