人胎盘CD133+细胞具有高增殖潜能集落形成细胞特性

目的 通过对人胎盘CD133⁺细胞群中高增殖潜能集落形成细胞(HPP-CFC)检测与生物学特性的分析，证明人胎盘存在早期造血干/祖细胞（HSPC）。 方法 采用机械法制备人胎盘组织（PT）单细胞悬液，用Histopaque-1007分离出单个核细胞(MNC)，经磁式分选（MACS）富集CD133⁺细胞，培养28 d后观察HPP-CFC集落形成能力，用流式细胞仪（FCM）对分选的细胞组份和HPP-CFC进行表型分析，实验全程用脐带血（UCB）作平行比较分析。 结果 培养28 d后，PT-CD133⁺与UCB-CD133⁺细胞组份分别扩增了266和362倍，前者低于后者（P<0.01）；PT-CD133⁺与UCB-CD133⁺细胞中HPP-CFC分别为(32.4±11.2)/5×10³、(17. 7±5.7)/5×10³，前者形成的HPP-CFC数量明显高于后者（P<0.01）；PT-CD133⁺、UCB-CD133⁺细胞培养至28 d时，除UCB-CD133⁺组的CD133⁺CD34^-亚群比例无明显改变外，CD133⁺CD34⁺、CD133^-CD34⁺和CD133⁺CD34^-（PT-CD133⁺组）亚型均比培养前减少。 结论 人胎盘组织CD133⁺细胞中存在HPP-CFC，说明胎盘CD133⁺细胞群中存在早期HSPC。     

IL-1β、TNF-α和IFN-γ引起的大鼠胰岛细胞凋亡及牛磺酸的影响

目的： 观察白细胞介素-1β(IL-1β)、肿瘤坏死因子-α（TNF-α）和γ-干扰素（IFN-γ）引起胰岛细胞凋亡、胰岛素分泌、Bcl-xL和Bax蛋白表达变化及其牛磺酸的影响。方法： 应用体外单层培养Wistar大鼠胰岛细胞，分别检测IL-1β、TNF-α和 IFN-γ对胰岛细胞凋亡细胞百分率、DNA片段、培养液中NO^-₂/ NO^-₃含量及NOS活性、胰岛素分泌、Bcl-xL和Bax表达的影响，并进一步观察牛磺酸的作用。结果： IL-1β、TNF-α和 IFN-γ联合可诱导胰岛细胞凋亡率明显增加，DNA明显片段化，同时NO^-₂/ NO^-₃含量和NOS活性亦明显升高，胰岛素分泌明显降低, Bcl-xL表达下降和Bax表达增强（P<0.01）；牛磺酸能阻断上述细胞因子的作用（P<0.01），并有一定的剂量依赖性。结论：牛磺酸能够改善IL-1β、TNF-α和 IFN-γ诱导的胰岛细胞凋亡，其机制可能与抑制NOS活性从而减少NO的生成以及下调Bax/Bcl-xL比例有关。     

转JAK2基因脐血CD34+细胞体外扩增与生物学特性研究

目的： 探讨转基因JAK2介导的脐血干祖细胞长期扩增调控的可行性和转基因细胞的生物学特征。方法: 构建逆转录病毒载体MGI-F₂JAK2，内含有JAK2基因的功能催化区和2个与小分子靶向基因合成药物(AP20187)结合的位点蛋白(F36v，F₂)。应用MiniMACS磁珠分选系统纯化分离脐血CD34⁺细胞，用含JAK2的逆转录病毒上清转染脐血CD34⁺细胞。转染后的CD34⁺细胞在IMDM培养体系中，将细胞分为AP20187组;FL组；TPO组；AP20187+FL+TPO (AFT) 组。对扩增后的细胞定期检测基因转移后GFP动态变化、细胞免疫标记、造血祖细胞集落培养、染色体核型分析和裸鼠致瘤实验。结果: 分选的CD34⁺细胞纯度>91%，基因转移率为49.32%±6.21%；只有AP20187+FL+TPO组可以使转基因的脐血CD34⁺细胞大量增殖，扩增至第8周时细胞数达10⁹，CD34⁺细胞GFP的阳性率由基线水平逐渐上升并于第8周时达到90%以上；细胞表型为CD33⁺、CD61⁺、Gly-A⁺部分阳性；CD38⁺、HLA-DR⁺强阳性；CD2、CD7、CD19接近阴性。扩增的CD34+细胞可分别形成BFU-E、CFU-GM、CFU-Mix并以CFU-GM集落为主。扩增后CD34⁺细胞检测染色体核型正常，裸鼠实验无致瘤特性。结论: 转染JAK2 基因的人脐血CD34⁺细胞协同FL和TPO细胞因子可以体外长期扩增脐血干祖细胞，对今后研究细胞信号转导、造血调控以及开展干细胞和基因治疗都有潜在的应用价值。     

干扰素-α联合GM－CSF诱导慢性髓性白血病细胞向树突状细胞分化

目的：研究干扰素-α（IFN-α）对慢性髓性白血病（CML）骨髓单个核细胞来源的树突状细胞（DCs）发育的影响。 方法： 12例初发慢性期CML患者的骨髓单个核细胞，分别与含如下细胞因子,RPMI-1640培养液共育：rhGM-CSF 1×106U/L联合rhIFN-α 2×106U/L（IFN-α组）、rhGM-CSF 1×10⁶U/L联合rhIL-4 5×10⁵U/L（IL-4组）、单用rhGM-CSF 1×10⁶U/L和单用rhIFN-α 2×106U/L，培养7 d；于第8-10 d，部分孔加入rhTNF-α 5×10⁴U/L。形态学（Wright染色、倒置显微镜）、免疫学（CD80、CD86、CD83、CD1a、HLA-DR）检测；磷脂酰丝氨酸（PS）转位检测 DCs凋亡情况；荧光原位杂交（FISH）对1例CML进行细胞遗传学分析；混合淋巴细胞反应（MLR）检测刺激同种异体T淋巴细胞增殖的能力。 结果： CML骨髓单个核细胞经上述细胞因子诱导7 d后，IFN-α组和IL-4组均呈现树突状细胞的典型形态；免疫学鉴定，IFN-α组DCs CD80、CD86、CD83、HLA-DR的表达显著高于IL-4组（P<0.05），经5×104U/L rhTNF-α作用后，两组DCs CD80、CD86、CD83、HLA-DR进一步上调，其中IFN-α组DCs CD80、CD86、CD83、HLA-DR的表达显著高于IL-4组（P<0.05）；经FISH证实来源于白血病细胞；两组DCs均具有刺激同种异体T淋巴细胞增殖的能力，IFN-α组刺激淋巴细胞增殖的能力明显高于IL-4组(P<0.05)。 结论： IFN-α可促进CML骨髓单个核细胞来源的树突状细胞的分化、活化。这可能是IFN-α在CML中的治疗机制之一。     

绿色荧光蛋白转基因小鼠CD34+/CD45+细胞在脊髓全横断大鼠模型中的存活及迁移

目的:探讨CD34⁺/CD45⁺细胞移植入脊髓全横断大鼠模型后的存活、迁移及分布情况。方法:体外培养绿色荧光蛋白（GFP）转基因小鼠骨髓细胞，经CD34、CD45单克隆抗体鉴定后移植入脊髓全横断大鼠模型脊髓横断处尾侧，分别在术后24 h、48 h、1周、2周、4周和8周行左心腔内灌注，取出脊髓，连续切片（片厚 10 μm），置于荧光显微镜下观察切片中有无绿色荧光细胞，并观察荧光细胞的分布范围；用免疫组化法检测CD34⁺/CD45⁺细胞的存活。 结果:脊髓横断处头尾两侧均可见绿色荧光细胞，且多分布于灰质中，散在或聚集成片；免疫组化法可见切片中有CD34⁺/CD45⁺细胞散在。 结论: CD34⁺/CD45⁺细胞可在脊髓全横断大鼠模型的脊髓中存活，并可迁移至脊髓横断处头侧，且随时间的延长迁移距离有所增加。     

乳腺癌患者外周血树突状细胞亚群及其HLA-DR表达的变化

目的：探讨乳腺癌患者外周血树突状细胞(DC)亚群和其HLA-DR表达变化及血浆中DC相关细胞因子水平的变化。方法:4色荧光流式细胞术分析57例乳腺癌术前、术后1周、术后6个月的患者及正常对照的外周血DC前体细胞pDC₁/pDC₂（CD11c+CD123-/CD11c-CD123+）比值及其HLA-DR的表达；酶联免疫吸附法检测血浆细胞因子白细胞介素-12p40（IL-12p40）、白细胞介素-10（IL-10）、γ-干扰素（IFN-γ）、白细胞介素-4（IL-4）水平。结果:57例乳腺癌患者中, 2例Ⅲ期、4例Ⅳ期外周血pDC缺乏，其余患者Ⅰ、Ⅱ、Ⅲ、Ⅳ期外周血pDC₁/pDC₂比值分别为1.62±0.59、1.41±0.63、0.91±0.32、0.81±0.29，均显著低于对照组（1.94±0.44,P<0.05）；Ⅰ、Ⅱ、Ⅲ期患者术后1周pDC₁/pDC₂比值为1.71±0.47、1.52±0.54、1.04±0.36，与术前比较均无显著差异（P>0.05），但显著低于对照组（P<0.05）; 术后6个月pDC₁/pDC₂比值分别为1.92±0.72、1.63±0.65、1.28±0.34，与术前比较，均有显著提高（P<0.05），但与对照组比较，仅Ⅰ期患者恢复正常（P>0.05）,Ⅱ、Ⅲ期患者仍然显著降低（P<0.05）。乳腺癌患者pDC亚群HLA-DR表达以及血浆中IL-12p40、 IL-10、IFN-γ、IL-4水平及IL-12p40/IL-10、IFN-γ/IL-4比值与对照组比较均无显著差异（P>0.05）。结论:Ⅰ-Ⅳ期乳腺癌患者外周血pDC₁/pDC₂比值降低，部分Ⅲ、Ⅳ期患者外周血pDC缺乏。pDC的HLA-DR表达及DC分泌相关细胞因子的能力没有同步变异。术后患者pDC亚群Ⅱ、Ⅲ期明显改善，Ⅰ期恢复正常。     

CD34+细胞的心肌细胞分化潜能研究

目的:了解粒细胞集落刺激因子(G-CSF)动员的CD34+细胞的心肌细胞分化潜能。方法:用异丙肾上腺素(ISO)复制急性心肌梗死大鼠动物模型,于3 h后用G-CSF动员骨髓造血干细胞进行心肌梗死动物模型的“自身干细胞移植”,用免疫组化和HE染色方法检测动物模型心梗区的CD34⁺细胞浸润以及心肌细胞再生情况。结果:用ISO后24 h,G-CSF处理组大鼠心梗区可见大量CD34⁺单个核细胞浸润,并有CD34⁺的新生心肌细胞生长,2周后疤痕组织不明显;而对照组心梗坏死区有大量以中性粒细胞为主的炎症细胞浸润,无CD34+细胞浸润及新生心肌细胞生长,2周后出现较大量的疤痕组织。结论:G-CSF动员CD34⁺细胞具有向心肌细胞分化的潜能,用G-CSF 动员造血干细胞的“干细胞自身移植”,可治疗急性心肌梗死。     

胆红素对大鼠急性肺损伤形成过程中氧自由基以及caspase-3表达的影响

目的： 探讨胆红素对抗急性肺损伤（ALI）形成的可能机制。方法: 健康雌性Wistar大鼠(190-210 g) 30只，随机分为生理盐水对照组、脂多糖（LPS）致ALI模型组、胆红素干预组。检测肺组织匀浆中羟自由基（OH^-）、过氧化氢(H₂O₂)和超氧阴离子自由基（O₂^·）含量以及肺组织中caspase-3表达的变化。结果: ①ALI模型组肺组织匀浆OH^-、H₂O₂、O₂^·含量及肺组织中caspase-3表达显著高于生理盐水对照组（均P<0.05）。②胆红素干预组肺组织匀浆OH^-、H₂O₂、O₂^·及肺组织中caspase-3表达明显高于ALI正常大鼠（均P<0.05），但少于ALI模型组（均P<0.05）。结论: ①胆红素能在一定程度上减少肺内凋亡细胞数量。②胆红素能减少ALI大鼠肺组织OH^-、H₂O₂、O₂^·水平。③ Caspase-3表达的变化有促脂多糖性肺损伤细胞凋亡作用。     

槲皮素和乙酸龙脑酯对细菌脂多糖诱导流产孕小鼠子宫组织中CD4+/CD8+ T细胞的影响

目的 探讨小鼠子宫组织中CD4⁺ 和CD8⁺ T细胞在早期胚胎丢失中的意义，研究槲皮素和乙酸龙脑酯对细菌脂多糖（LPS）诱导流产小鼠的保胎效果和对母胎界面免疫平衡的调节作用。 方法 采用LPS尾静脉注射，制造小鼠流产模型，孕4～7d分别口服不同保胎药物，用药前后检测各组（n=10）小鼠子宫组织CD4⁺/CD8⁺T细胞亚群的变化。 结果 LPS促流产后，小鼠子宫壁CD4+T细胞数量显著增多（P<0.01），CD8⁺ T细胞无明显变化（P>0.05），CD4⁺/CD8⁺比值显著升高（P<0.01）。预先口服保胎药物能不同程度抑制LPS的作用。其中以槲皮素和乙酸龙脑酯联合使用组的保胎效果最为明显，CD4^+/CD8⁺比值下降，较LPS流产模型组差异极显著（P<0.01）。 结论 小鼠子宫组织CD4^+/CD8⁺比值升高与早期胚胎丢失关系密切，槲皮素和乙酸龙脑酯能够调节小鼠子宫局部的免疫微环境，从而起到一定的促孕保胎作用。     

类风湿关节炎CD4+CD28-T细胞与淋巴细胞凋亡的相关性研究

目的: 研究类风湿关节炎(RA)患者外周血CD4⁺CD28^-T细胞比例与淋巴细胞凋亡异常的相关性。方法: 采用流式细胞术三色分析法检测50例患者和50例健康志愿者的外周血淋巴细胞中CD4⁺CD28^-T细胞比例;通过加入PHA孵育检测RA病人外周淋巴细胞和正常对照的淋巴细胞对激活诱导细胞死亡(AICD)易感性差异;分析CD4⁺CD28^-T细胞比例与外周血淋巴细胞凋亡率的相关性。结果: RA组CD4⁺CD28^-T细胞比例的均数明显高于健康对照组(7.79%±3.52% vs 1.89%±1.78%,P<0.05)。RA组病人外周血淋巴细胞的AICD凋亡率低于健康对照组(11.38%±5.73% vs 19.46%±6.32%,P<0.05)。Spearman相关分析结果显示CD4⁺CD28^-T细胞比例与外周血淋巴细胞AICD凋亡率负相关(r=-0.433,P<0.01)。结论: RA患者外周血中CD4⁺CD28^-T细胞比例增多,活化淋巴细胞生存期延长,这可能参与RA的发病机制。     

人源化NOD/SCID小鼠免疫细胞的动态变化与鉴定

目的： 比较脐血干细胞与单个核细胞移植NOD/SCID鼠所建立的人源化SCID模型，分析人源化淋巴细胞重建。方法： 磁珠分选法分离脐血中CD34⁺细胞，淋巴细胞分层液分离脐血单个核细胞，分别经尾静脉输入NOD/SCID小鼠。每隔2周采血至10周，流式细胞术动态检测人源淋巴细胞CD45、CD19、CD3抗原。第10周处死小鼠收集外周血、骨髓、胸腺组织，RT-PCR检测模型鼠组织中人β₂M基因及RAG2基因。结果： 两种类型细胞移植均可重建人源免疫细胞，人源淋巴细胞表达水平均在第8周达高峰。骨髓中人源淋巴细胞表达水平明显高于外周血。RT-PCR在外周血与骨髓检测到人β₂M基因及RAG2基因标志。结论： CD34⁺细胞移植重建人源化NOD/SCID免疫系统模型效果要好于脐血单个核细胞。人源T淋巴细胞在模型鼠骨髓中分化成熟。     

从G-CSF动员的外周血细胞悬液培养的成纤维细胞样细胞的特性分析

目的： 研究从G-CSF动员的外周血细胞（PBC）悬液培养的成纤维细胞样（F-L）细胞的特性。 方法： 取PBC中贴壁细胞分4组培养：①RPMI-1640组；②L-DMEM组；③粒细胞集落刺激因子（G-CSF）组；④白细胞介素-3（IL-3）组。流式细胞仪分析各组培养的F-L细胞特性。 结果： 培养2-3周后，4组均能收获到F-L细胞，细胞贴壁生长，但不融合，不能连续传代培养，③④组细胞数量明显多于①②组，4组F-L细胞表型相似：CD33+、CD11c+、CD64+、CD14+、CD45+、HLA-DR+、CD86+、CD34-、CD38-、CD3-、CD19-、CD56-、CD29-、CD44-、CD105-；与单核细胞（PB-M）表型差异仅CD38表达不同而与间质干细胞（MSC）或树突状细胞（DC）表型明显不同。 结论： 从PBC培养的F-L细胞为巨噬细胞，不是MSC或DC；G-CSF、IL-3能提高F-L细胞培养数量，不改变PB-M向巨噬细胞分化的分化方向。     

The sensitivity of IL-4 production for cAMP inducers is lost in CD4+ T cells from aged mice

CD4⁺ T cell clones have been demonstrated to display a differentialsensitivity for the induction of cAMP. In the present studywe investigated whether the differential sensitivity of CD4⁺T cell clones for cAMP inducers is also applicable to freshlyisolated phenotypically and functionally distinct CD4⁺ T cellsubsets that develop naturally in aging mice. Our results showthat the concanavalin A induced and anti-CD3 induced proliferativeresponse of CD4⁺ T cells from young mice is more sensitive forprostaglandin E₂ (PGE₂) and forskolin than that of their agedcounterparts, although the IL-2 production by these cells wasequally sensitive. In contrast, only a slight or no inhibitoryeffect of these cAMP inducers was found when the cells werestimulated with the combination of phorbol myristate acetateand lonomycln. In contrast to the findings obtained with T_n2clones, IL-4 production by freshly isolated CD4⁺ T cells wasinhibited by the cAMP inducers, whereas exogenous IL-2 had norestorative effect. However, the IL-4 production by CD4⁺ T cellsfrom aged mice was less sensitive than the IL-4 production byCD4⁺ T cells from young mice, although CD4⁺ T cells from agedmice showed significantly higher levels of intracellular cAMPin response to PGE₂. These higher levels of cAMP were relatedto the increased fraction of memory cells in aged mice: theMel-14^– Pgp-1⁺⁺ CD4⁺ T cells responded with at least 2-foldhigher levels of intracellular cAMP than the naive cells inyoung as well as in aged mice. Although memory CD4⁺ T cellsfrom young as well as aged mice responded vigorously to PGE₂by an enhancement of intracellular cAMP, only the IL-4 productionby cells from young mice was significantly inhibited. Therefore,it is not likely that the induction of cAMP is a major eventin the skewing of a primary response towards a T_h2 type of response.     

T cell subpopulation phenotypes in filarial infections: CD27 negativity defines a population greatly enriched for Th2 cells

Three-color flow cytometric analysis was used to define surfacemarkers which identify the T_h2-type CD4⁺ cells responsible forthe eosinophilia and elevated serum IgE typical of tissue invasivehelminth infections. A group of six mAba to well known cellsurface markers were screened for differential expression onCD4⁺ CD45RO⁺ lymphocytes from normal individuals (NL; n = 6)and filaria-infected patients (PT; n = 10). The majority ofmarkers were expressed equally by both groups, but the CD4⁺CD45RO⁺ cells in the PTs showed significantly higher levelsof expression of HLA-DR than those of NLs (P = 0.014). ThisCD4⁺ HLA-DR⁺ subpopulation was then studied further for itsexpression of an additional 10 activation and adhesion molecules.CD27 showed a trend for lower intensities of expression on PTCD4⁺ HLA-DR⁺ cells than on those of NLs. Analysis of the serumfrom both NLs and PTs revealed that PTs had significantly higherlevels of soluble CD27 and CD25 (IL-2R) In the serum than NLs(P < 0.01 and P = 0.022 respectively) indicating a generalstate of Immune activation and differentiation. Functional analysisof the CD4⁺ HLA-DR⁺ and the CD4⁺ CD27^– subpopulatlonsrevealed that the CD4⁺ HLA-DR⁺ cells produced significantlyhigher levels of IL-5 than the CD4⁺ HLA-DR^– cells (P <0.04), and the CD4⁺ CD27^– cells produced significantlyhigher levels of both IL-4 and IL-5 than the CD4⁺ CD27^–cells (P <0.05 and P <0.001 respectively). Thus, whilethe CD4⁺ CD27^– and CD27⁺ subpopulatlons contain T_h1 andT_h0 cells, only the CD4⁺ CD27^– population contains theT_h2 cells (producing both IL-4 and IL-5).     

Interleukin 10 inhibits T cell alloreaction induced by human dendritic cells

Human dendritic cells (DC) generated from CD34⁺ hematopoieticprogenitors cultured in the presence of granulocyte macrophagecolony stimulating factor (GM-CSF) and tumor necrosis factor(TNF)- are related to Langerhans cells (DLC) and have been shownto induce a strong proliferation of allogeneic CD4⁺ T cells.The present study shows that recombinant human IL-10 (h-IL-10)inhibits the primary and secondary proliferative responses ofboth CD4⁺ and CD8⁺ T cells induced by allogenelc CD1a⁺ DLC.The alloreaction induced by DLC generated after 5–18 daysof culture of CD34⁺ HPC was equally inhibited by h-IL-10, thusindicating that DLC were sensitive to h-IL-10 at all stagesof differentiation. This is further indicated by the h-IL-10-inducedinhibition of the T cell alloreaction mediated by interdigitatingDC freshly isolated from tonsils. h-IL-10 specifically actedon DLC as it did not affect the proliferation induced by Epstein-Ban-viruslymphoblastoW cell lines (EBV-LCL) nor that induced by immobilizedanti-CD3. The inhibitory effect of h-IL-10 was not due to theproduction of suppressive factors by the DLC, as the additionof DLC and IL-10 did not inhibit EBV-LCL-induced T cell proliferation.Rather, the inhibition of cytokine production (IL-2, GM-CSF,TNF, IFN-) observed after 24 h of co-culture may explain theinhibition of T cell DNA synthesis detected 3 days later. Theh-IL-10-lnduced inhibition of human DC mediated alloreactionadvocates considering the use of h-IL-10 In the prevention oftransplant refection and graft versus host disease, phenomenainitiated by DC.     

Superantigen-reactive T cells that display an anergic phenotype in vitro appear functional in vivo

Clonal deletion and/or inactivation establishes tolerance toself antigens. Endogenous and exogenous (bacterial) superantigens,like the staphylococcal enterotoxlns, induce ligand-specificclonal anergy in vivo and thus are believed to mirror aspectsof post-thymic tolerance mechanisms in mature peripheral T cells.Here we analyzed the level of anergy of ligand-responsive V_ß8⁺T cells from staphylococcal enterotoxin B (SEB)-primed micein vivo and in vitro. Upon in vitro restimulation with SEB,CD4⁺V_ß8⁺ and CD8⁺V_ß8⁺ T cells failed toproduce IL-2. However, functional IL-2 receptors were triggered,since supplementation with IL-2 induced clonal growth in virtuallyall CD4⁺V_ß8⁺ and CD8⁺V_ß8⁺ T cells as determinedby limiting dilution analyses. Thus in vitro unresponslvenessof lymphocytes from SEB-primed mice reflects the inability ofSEB-reactlve V_ß8⁺ T cells to produce IL-2. Surprisingly,anergy as defined in vitro was at variance with that in vivo.Following further challenge with SEB, systemic and acute lymphokineproduction (Including IL-2 and tumor necrosis factor) occurredwith almost identical peak values and kinetics to primary invivo responses, and D-galactosamlne-sensltlzed mice succumbedto lethal shock. Polymerase chain reaction analyses revealedthat CD4⁺V_ß8⁺ expressed IL-2-specific mRNA in vivoupon restimulatlon with SEB. While lymphokine production andexpression of the IL-2 receptor was similar to the responseto in vivo primary stimulation, only CD8⁺V_ß8⁺ T cellsexpanded clonally upon reintroductlon of SEB in vivo. Henceprimed V_ß8⁺ T cells challenged with SEB display invitro anergy yet in vivo responsiveness, at least in part. Weconclude that the state of anergy is reversible, dependent uponthe quality of activation signals provided in in vivo ratherthan in in vitro culture conditions.     

Interferon-γ and interleukin-4 reciprocally regulate the production of monocytes/macrophages and neutrophils through a direct effect on committed monopotential bone marrow progenitor cells

We studied the direct effects of interferon-γ (IFN-γ) in single cell colony assays of CD34⁺HLA-DR++ bone marrow progenitor cells stimulated by either granu-locyte-colony-stimulating factor (G-CSF), interleukin(IL)-3, granulocyte/macro-phage-colony-stimulating factor (GM-CSF), combinations of these CSF or medium conditioned by the 5637 human bladder carcinoma cell line. In this culture system IFN-γ stimulated monocytic colonies (CFU-M) no matter which CSF or CSF combination was used to support them and inhibited granulocytic colonies (CFU-G) if they were generated in the presence of G-CSF. IL-4 antagonized the myelopoietic effects of IFN-γ: the IFN-γ induced suppression of G-CSF-supported CFU-G, as well as the stimulation of CFU-M, were reversed by IL-4. In all cultures, IFN-γ had a limited, but statistically non-significant, inhibitory effect on CFU-GM, which was not affected by the presence of IL-4. These data show that IFN-γ and IL-4 reciprocally regulate the generation of myeloid cells involved in humoral (neutrophils) and cellular (macrophages) immune responses through a direct effect on monopotential myeloid progenitor cells.     

地塞米松对实验性哮喘小鼠TH1/TH2细胞因子的影响及其机制的探讨

目的：初步探讨地塞米松对小鼠哮喘模型哮喘进展过程中T_H细胞因子的影响及其机制。方法： 18只BALB/c小鼠随机分为正常对照组、哮喘组和地塞米松处理组，每组各6只。运用流式细胞仪检测小鼠脾细胞胞内细胞因子白细胞介素-4和干扰素-γ的表达,用Western blotting方法检测各组小鼠肺组织转录因子 T-bet 和GATA-3的表达，用组织学观察肺组织炎症程度。结果：哮喘鼠T细胞内IL-4/IFN-γ比值明显高于正常组（P﹤0.01）；地塞米松组细胞内IL-4/IFN-γ比值明显低于哮喘组（P﹤0.01）。哮喘组肺组织T-bet的表达明显低于正常对照组（P﹤0.01），GATA-3明显高于正常对照组（P﹤0.01）;地塞米松组的小鼠肺组织T-bet和GATA-3的表达均明显低于哮喘组（P﹤0.01）， GATA-3降低更为明显。结论：调控T_H1和T_H2细胞转化过程中重要转录因子T-bet和GATA-3的表达，可以改变IL-4/IFN-γ比值，纠正哮喘的T_H2漂移，从而改善相应的炎性症状，这可能是地塞米松抑制哮喘的重要机制之一。