rhBMP-2对再生障碍性贫血小鼠骨髓造血恢复的促进作用

探究了人重组骨形态发生蛋白-2(rhBMP-2)对再障小鼠的治疗作用。采用5-FU联合白消安建立小鼠再障模型,通过干预rhBMP-2进行治疗。考察了各实验组小鼠白细胞数、骨髓单核细胞数、体重、存活率、脾系数、粒系-巨系细胞集落(CFU-GM)数以及骨髓单核细胞中CD34+细胞比例,进行股骨、脾脏HE切片分析。结果表明,相较于再障对照组,rhBMP-2治疗组小鼠的白细胞数、存活率、CFU-GM集落数及骨髓单核细胞数显著提高,并且骨髓单核细胞中的CD34+细胞含量也提高,显著改善脾脏功能和缓解骨髓抑制,证实rhBMP-2能够促进再障小鼠造血损伤的修复。     

刺五加增强小鼠免疫功能的作用

研究了刺五加对正常小鼠及免疫抑制小鼠免疫器官重量，细胞数目和体视学参数的影响。结果表明，ＡＳ能增强小鼠脾脏和肠系膜淋巴结的重量，细胞数目，脾脏白髓体积和淋巴结皮质总体积。ＡＳ尚能明显对抗环磷酰胺所致的免疫抑制作用。揭示ＡＳ有增强小鼠免疫功能的作用。     

大鼠脾不统血证模型免疫器官—免疫细胞的变化

Wister大鼠灌胃酒醋及阿斯匹林,造成脾不统血征(上消化道出血)动物模型。结果:模型组动物中枢免疫器官胸腺皮质的淋巴细胞减少,髓质PAS阳性物质减少;周围免疫器官脾脏T细胞区和B细胞区缩小。免疫细胞白细胞、红细胞、血小板减少,RBc-c_3b受体花环率、RBc-IC花环率降低,与对照组动物比较有显著性差异。经归脾丸及其加味反证治疗,病变得以恢复。提示脾化生之气血为免疫的物质基础。     

健康恒河猴外周血及肠系膜淋巴结中树突状细胞(Dendritic Cell)的亚群及分布特点

树突状细胞(Dendritic Cell,DC)作为天然免疫的重要组成部分,在抗原识别和抗原呈递过程中发挥重要作用.对DC细胞在恒河猴外周血及淋巴结组织中的细胞亚群及其分布频率进行初步观察.取健康源恒河猴外周血和肠系膜淋巴结,从中分离出淋巴细胞.利用流式细胞术检测分析不同亚群的DC细胞在其间的分布.结果表明,外周血及淋巴结中DC细胞比例均较低,但外周血中DC比例略高于肠系膜淋巴结.mDC亚群占总DC细胞数比例高于pDC细胞亚群,而肠系膜淋巴结中mDC比例相较外周血中有明显下降,统计学差异显著.测定了健康源恒河猴各亚群DC细胞在外周血和淋巴组织中的基础数值,为相关模型研究奠定了基础.     

中华鳖白细胞发生的观察

通过对中华鳖骨髓、脾脏、肝脏、肾脏及外周血等几种组织涂片或印片的观察研究，发现骨髓是中华鳖粒细胞的主要发生器官，而脾脏是中华鳖淋巴细胞和单核细胞的主要发生器官，白细胞的发育过程大致经过3个阶段，即原始阶段、幼稚阶段、成熟阶段，着重描述了各个阶段细胞的形态特征．     

鳖的肝脾是免疫器官

取鳖的各类骨,肝,脾制成切片进行研究。结果发现：鳖骨髓不造血,肝内的淋巴组织多为成熟的中、小淋巴细胞,少数为分裂状态的淋巴细胞和浆细胞,肝实质内,肝窦内及靠近肝内的血管处,各期各类的血细胞丰富;脾脏内的脾小体中,越靠近中心淋巴细胞,其核仁越清晰,细胞核的结构越疏松,细胞的分裂现象越明显,脾索内发现有巨噬细胞,网状细胞,浆细胞,成熟和幼稚的各种血细胞等,因此说,肝和脾是鳖的免疫器官。     

OX40L在小鼠B16黑素瘤细胞中表达及对活化淋巴细胞凋亡影响

目的:构建OX40L的真核表达载体,分析其在B16细胞中的表达,研究OX40L对活化T淋巴细胞凋亡的影响.方法:以小鼠C57BL/6脾脏的cDNA为模板,PER扩增小鼠OX40L基因,构建真核表达载体pVAX1-OX40L,转染B16细胞后,荧光染色检测OX40L的表达;利用AnnexinV-PE凋亡试剂盒,检测B16黑素瘤细胞-淋巴细胞体外混合培养中对活化淋巴细胞凋亡的影响.结果:成功构建OX40L的真核表达载体,并转染B16细胞中,流式细胞术和激光共聚焦显微术均可检测到OX40L表达于B16细胞表面.淋巴细胞体外混合培养显示,表达OX40L的B16细胞组活化淋巴细胞的凋亡率为6.57%,而空质粒转染组为17.24%.结论:OX40L能表达于B16细胞表面,并能显著抑制活化淋巴细胞凋亡.     

淫羊藿对RANKL、M-CSF诱导的破骨样细胞形成及FN表达的影响

建立RANKL、M-CSF诱导的破骨样细胞体外培养体系,采用细胞染色分析研究淫羊藿对RANKL和M-CSF诱导全骨髓细胞分化形成破骨样细胞的作用,并探讨FN在破骨样细胞形成过程中的作用,结果显示,淫羊藿能够抑制RANKL、M-CSF诱导的破骨样细胞的形成,FN与破骨样细胞的融合有关.     

熊果酸对H22荷瘤小鼠抗肿瘤及免疫调节作用

目的 探讨熊果酸（UA）对H22荷瘤小鼠抗肿瘤作用及免疫功能的影响.方法 皮下移植建立H22荷瘤小鼠模型,腹腔注射不同剂量UA,检测抑瘤率和免疫器官指数,MTT法检测脾脏T、B淋巴细胞增殖能力,流式细胞术检测CD4＋、CD8＋T细胞亚群含量及比例,ELISA法检测血清细胞因子IL-2、IL-4和TNF-α的表达量.结果 UA对小鼠皮下移植性肿瘤H22有显著的抑制作用,可降低免疫器官中异常增大的脾指数,增强脾脏中T、B淋巴细胞增殖能力,提高淋巴细胞亚群CD4＋T细胞表达及CD4＋/CD8＋T细胞亚群比例,促进血清IL-2、TNF-α表达,降低IL-4表达.结论 UA可抑制小鼠肝癌H22肿瘤生长,体内可以提高荷瘤小鼠的免疫能力,其抗肿瘤作用可能与机体的免疫调节作用相关.     

PPARα在器官移植中的作用初探

目的:探讨PPARα在器官移植中的作用。方法:C57BL/6J经口给予非诺贝特或者Wy14643,连续7 d,取脾脏,同时取BALB/c小鼠的脾脏,分离脾细胞进行混合淋巴细胞反应。结果:经过非诺贝特或者Wy14643处理的小鼠,其脾细胞在混合淋巴细胞反应中表现为无应答。结论:非诺贝特或者Wy14643激活的PPARα具有抑制混合淋巴细胞反应的作用。     

Continued RAG expression in late stages of B cell development and no apparent re-induction after immunization.

Models of B-cell development in the immune system suggest that only those immature B cells in the bone marrow that undergo receptor editing express V(D)J-recombination-activating genes (RAGs). Here we investigate the regulation of RAG expression in transgenic mice carrying a bacterial artificial chromosome that encodes a green fluorescent protein reporter instead of RAG2. We find that the reporter is expressed in all immature B cells in the bone marrow and spleen. Endogenous RAG messenger RNA is expressed in immature B cells in bone marrow and spleen and decreases by two orders of magnitude as they acquire higher levels of surface immunoglobulin M (IgM). Once RAG expression is stopped it is not re-induced during immune responses. Our findings may help to reconcile a series of apparently contradictory observations, and suggest a new model for the mechanisms that regulate allelic exclusion, receptor editing and tolerance.     

中华鳖红细胞发育过程的观察

通过骨髓、脾脏、肝脏、肾脏和外周血等器官涂片或印片观察来探讨中华鳖红细胞的产生器官、发育场所和发育各阶段的特征。结果表明骨髓是中华鳖红细胞的发源地，骨髓和脾脏是红细胞成熟的主要场所，在外周血和脾脏中亦可见少量未成熟或正在有丝分裂的红细胞，红细胞发育经过原始、幼稚和成熟等三个阶段，着重描述了红细胞发育各阶段的主要形态特征。     

14MeV快中子辐照对大鼠免疫系统的损伤

用14 MeV快中子对Wistar雄性大鼠进行5 Gy的全身照射,观察其免疫系统损伤情况及氧化应激的相关变化.大鼠分为辐射组和对照组,分别在辐射后1,7,14d 3个时间点取血液、胸腺和脾脏进行研究.结果表明,辐照后第1d,辐照组大鼠白细胞和淋巴细胞数量降至最低,照后第7、14d有所恢复,但仍不足正常组的1/2.血小板数在照后第1d开始减少,至第7d达到最低值,第14d仍与正常组有显著差异.而大鼠骨髓有核细胞总数辐照后14d明显低于正常组.另外胸腺和脾脏均出现萎缩,脏器指数明显减小.血浆、胸腺和脾脏的总抗氧化能力T-AOC、SOD酶活性及MDA值含量均有不同程度的升高趋势.说明快中子辐射影响血浆、胸腺和脾脏的抗氧化应激能力,诱导细胞凋亡或坏死,造成胸腺和脾脏的萎缩以及一系列组织形态的改变,从而严重影响大鼠的正常免疫功能.      

Mature murine B lymphocytes immortalized by Kirsten sarcoma virus

Clonal, antigen-specific, functionally responsive cell populations have proved critical for the analysis of the activation and regulation of lymphocytes. Such studies with B lymphocytes, the precursors of antibody-secreting cells, are hampered by the difficulty in generating phenotypically mature, antigen-reactive lines from defined cell populations. One method is to use acutely transforming retroviruses, which can transform B-lineage lymphocytes in vitro. However, Abelson murine leukaemia virus (A-MuLV) infection of murine bone marrow cells in vitro yields mostly immature B-cell lines, and infection of murine bone marrow cells with murine sarcoma viruses carrying ras related genes produces only immature lymphoid cell lines. Retroviruses which contain ras can immortalize nonlymphoid cells without causing loss of mature phenotypic characteristics. We used ras-containing Kirsten sarcoma virus (KiSV) pseudotyped with an amphotropic MuLV helper virus, to infect a purified population of mature, hapten-binding murine splenic B lymphocytes, aiming to generate mature B-cell lines to use as models for the study of B-cell growth and differentiation physiology. Immortalized B-cell lines which retain the same mature phenotype as the starting population, including hapten-specific binding, were produced. This is the first demonstration of a method for immortalizing selected antigen-binding B lymphocytes, and the first example of immortalization of mature B cells in vitro with an acutely transforming ras-containing retrovirus.     

Spleen colony-forming cell as common precursor for tissue mast cells and granulocytes

The haematopoietic stem cells which produce colonies in the spleen of irradiated mice (CFU-S) can differentiate into erythrocytes, granulocytes, megakaryocytes and B lymphocytes. Although mast cell precursors are known to be present in the bone marrow, spleen, fetal liver and peripheral blood of mice, the relationship between the mast cell precursor and CFU-S has remained unclear. We have now made use of mice of two mutant genotypes to determine whether or not the tissue mast cell is a progeny of CFU-S. Giant granules of beige (C57BL/6-bg/bg, Chediak-Higashi syndrome) mice can be used for identification of the origin of both tissue mast cells and granulocytes, and WBB6F1-W/Wv mice are useful recipients because they lack tissue mast cells owing to a defect in mast cell precursors. We injected the cells from a single spleen colony into each WBB6F1-W/Wv mouse and demonstrated directly that the tissue mast cell is a progeny of CFU-S.     

家兔B细胞的最早来源部位

采用光镜和电镜技术对不同发育时期的家兔肝脏、骨髓和阑尾中的Ｂ细胞及其动态变化进行了系统观察，结果表明，家兔的胚肝可能是Ｂ细胞最早发生和分化的场所，可能具有与鸟类法氏囊类似的功能．家兔阑尾的淋巴组织在出生后逐渐发育形成，与鸟类法氏囊滤泡髓质部的形成不同，因此，阑尾可能不是Ｂ细胞的最早来源部位，而是外周淋巴器官．     

Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1

Adaptive immunity depends on T-cell exit from the thymus and T and B cells travelling between secondary lymphoid organs to survey for antigens. After activation in lymphoid organs, T cells must again return to circulation to reach sites of infection; however, the mechanisms regulating lymphoid organ exit are unknown. An immunosuppressant drug, FTY720, inhibits lymphocyte emigration from lymphoid organs, and phosphorylated FTY720 binds and activates four of the five known sphingosine-1-phosphate (S1P) receptors. However, the role of S1P receptors in normal immune cell trafficking is unclear. Here we show that in mice whose haematopoietic cells lack a single S1P receptor (S1P1; also known as Edg1) there are no T cells in the periphery because mature T cells are unable to exit the thymus. Although B cells are present in peripheral lymphoid organs, they are severely deficient in blood and lymph. Adoptive cell transfer experiments establish an intrinsic requirement for S1P1 in T and B cells for lymphoid organ egress. Furthermore, S1P1-dependent chemotactic responsiveness is strongly upregulated in T-cell development before exit from the thymus, whereas S1P1 is downregulated during peripheral lymphocyte activation, and this is associated with retention in lymphoid organs. We find that FTY720 treatment downregulates S1P1, creating a temporary pharmacological S1P1-null state in lymphocytes, providing an explanation for the mechanism of FTY720-induced lymphocyte sequestration. These findings establish that S1P1 is essential for lymphocyte recirculation and that it regulates egress from both thymus and peripheral lymphoid organs.