虎纹蛙外周血细胞的超微结构

目的：观察虎纹蛙外周血细胞的超微结构。方法：运用透射电镜技术。结果：在外周血细胞中可区分出红细胞,单核细胞,淋巴细胞,中性粒细胞,嗜酸性粒细胞,嗜碱性粒细胞和血小板细胞。与哺乳纲动物不同,虎纹蛙白细胞表面均有伪足。结论：脊椎动物白细胞形态结构的分化程度可能与动物的分类地位有关。     

白细胞介素8的产生及其分子生物学概况

IL-8是一种新命名的细胞因子,主要产自血单核细胞,但T细胞、内皮细胞、纤维母细胞等亦可产生。其主要成熟分子形式为一72个氨基酸的单肽链,对T 细胞、中性粒细胞有强烈的趋化作用。在T 细胞、中性粒细胞、嗜碱性粒细胞及单核细胞表面有与其对应的受体,因此,其对淋巴细胞再循环、炎症反应等具有重要的调节效应。     

多态性FcγRⅡ基因定位于人类第1号染色体长臂(1q)上

人类白细胞表面的Fc受体(FcγR)是免疫应答过程中将体液免疫系统同细胞效应功能结合起来的重要组分,根据其分子大小,对IgG的亲和力、细胞分布类型及体外功能FcγR至少可分为3大类。人类FcγRⅡ则是表达于单核细胞、血小板、嗜酸性粒细胞、B细胞及中性粒细胞表面的一种分子量为40000的糖蛋白,它可结合寡聚体形式的人IgG及小鼠IgGl和IgG2b,同时有证据表明单核细胞FcγR Ⅱ     

乙型流感患者外周血白细胞和淋巴细胞亚群变化分析

目的 探讨乙型流感患者外周血白细胞和淋巴细胞亚群的变化特点,为乙型流感的诊断、治疗和预后判断提供实验室依据.方法 采用全血细胞分析和流式细胞分析法分别检测47例乙型流感患者急性期和恢复期的外周血白细胞及淋巴细胞亚群,并与38名健康人比较.结果 乙型流感轻症患者外周血白细胞总数在急性期显著下降,恢复期迅速上升,而重症患者外周血白细胞总数、中性粒细胞百分比及绝对值在急性期显著上升,恢复期迅速下降;所有乙型流感患者淋巴细胞总数、CD3、CD4、CD8、CD19在急性期显著下降,恢复期迅速上升;轻症患者的NK细胞绝对值在急性期与恢复期都与健康对照组无显著差异,而重症患者NK细胞绝对值在急性期显著下降,恢复期迅速上升.结论 乙型流感患者在急性期出现白细胞总数及中性粒细胞的显著上升,而NK细胞绝对值的大幅降低可以提示病情重症化倾向.     

淋巴细胞增生反应、IL2产生和IL2受体表达三者相关性的初步研究

<正> 检测T淋巴细胞功能最常用的方法是有丝分裂原刺激细胞DNA合成的细胞增殖试验。近年来已开始研究细胞合成分泌白细胞介素 2(IL 2)和细胞膜表达IL 2受体的功能。细胞产生 IL 2、表达IL 2受体以及DNA合成三者之间的关系如何?引起了注意。作者从以下四个方面:①不同剂量刀豆蛋白A(Con A)刺激小鼠脾细胞;②Con A刺激胸腺细胞;③中药冬虫夏草刺激小鼠脾细胞;以及④中药雷公藤对 Con A诱生脾细胞免疫反应的抑制作用,初步探讨三种反应之间的关系。     

瘦素与免疫应答

痩素作为一种激素样细胞因子,在造血及免疫细胞的发育中发挥重要作用。它主要作用在造血干、祖细胞阶段,从而引起三系造血细胞增殖,特别是对淋巴细胞的生成具有重要的促进作用,并在维持胸腺CD4 CD8 T细胞成熟的过程中发挥作用。痩素通过与表达在单核巨噬细胞、中性粒细胞、NK细胞、淋巴细胞表面的长型受体结合,促进上述免疫细胞的活化增殖,释放细胞因子,特别是促进Th1型促炎症免疫应答。     

基于Sugeno型模糊神经网络的外周血白细胞自动分类研究

血白细胞分类计数嗜碱性粒细胞、嗜酸性粒细胞、中性粒细胞、淋巴细胞、及单核细胞是临床诊断的重要依据。作者在细胞图像分割、白细胞特征提取、白细胞特征选择后,提出了用Sugeno型模糊神经网络的方法实现外周血白细胞的自动形态学分类。用构建的网络分别进行白细胞的3分类和5分类试验,结果表明,用模糊神经网络分类器对血白细胞形态学分类可行。     

人活化T淋巴细胞通过细胞间直接接触激活致敏嗜中性粒细胞

活化T 淋巴细胞可通过其膜表面结合分子与嗜中性粒细胞直接作用,激活嗜中性粒细胞,或使之处于一种致敏状态,增加其对其它刺激的敏感性,从而增强嗜中性粒细胞在抗微生物免疫和组织损伤中的作用。以贴壁法去除单核细胞,尼龙毛吸附去除B 细胞,从正常人外周血PBMC 中得到纯     

041 儿童哮喘早期免疫应答反应及调控机制

病毒感染引起的儿童哮喘早期免疫反应中,Th1细胞下调及功能降低;Th2细胞发挥主要作用,驱使嗜酸性粒细胞在肺中的募集.CD8+T细胞及NK细胞调控Th2细胞分化及其分泌细胞因子.不成熟的抗原提呈系统(APC)导致免疫应答向Th2型反应发展.CD14作为脂多糖(LPS)受体决定早期APC系统的成熟.     

青少年型葡萄糖脑苷脂病一例

患者　女,16岁,因脾脏肿大入院。查体:营养中等,皮肤未见出血点及紫斑,黏膜未见出血点,胸骨无明显压痛,淋巴结未扪及肿大。血常规检查:白细胞10 .3×10 9/ L ,红细胞3.5 5×10 1 2 / L,血色素12 0 g/ L,血小板2 5 0×10 9/ L。中性杆状核粒细胞0 .5 4 ,成熟淋巴细胞0 .35 ,单核细胞0 .0 1,嗜酸性粒细胞0 .1。未见有核红细胞及幼稚细胞。骨髓象:骨髓有核细胞增生明显活跃,粒红比为4 .5∶1,粒系细胞明显增生,各期细胞均见,形态比值正常。嗜酸性粒细胞占13%。红系增生,各期细胞均见,形态比值基本正常。成熟红细胞形态大小正常。淋巴细胞系正…     

Quantitation of the number of mitogen molecules activiting DNA synthesis in T and B lymphocytes

Thymus-derived (T) and bone-marrow-derived (B) lymphocytes bound equal numbers of Concanavalin A (Con A) molecules, although only T cells were stimulated to proliferation by soluble Con A. Optimal T cell proliferation occurred when approximately 3 × 10⁶ molecules of Con A were bound per cell, which corresponds to 3–10% of the available receptors. Con A can be converted to a selective B cell mitogen provided it was presented to the cells in a locally concentrated form, achieved by cross-linking the lectin to the bottom of tissue culture Petri dishes. Optimal B cell stimulation by insolubilized Con A was obtained at a density of 1–4 × 10¹² molecules/cm.² It was estimated that per unit surface area, B and T cells were activated by the same number of Con A molecules, whereas T cells required more molecules per cell. In terms of T–B cell co-operation this suggests that optimally activated T cells present an optimally stimulating number of Con A molecules to the B cells by direct cell to cell interaction.

It is postulated that the actual interaction between Con A and the sugar containing receptor at the cell membrane is not directly responsible for lymphocyte activation, but as a consequence of this initial binding, the Con A-receptor complex interacts with a second membrane receptor of a different type. When a sufficient number of these second receptors have reacted with the Con A-sugar receptor complex the cell became activated. T cells are postulated to have a greater number of the second type receptors than B cells. The ability of locally concentrated Con A to activate B cells but not T cells is explained in terms of this hypothesis.

     

人胃癌细胞系和成纤维细胞的COn A受体分布的变异

本文采用 Con A-过氧化物酶光镜和电镜细胞化学方法观察了体外培养的人胃癌细胞(MGC80-3)和成纤维细胞质膜的 Con A 受体分布特点,未经固定的 MGC80-3细胞,Con A 受体复合物呈斑块样不规则分布,而成纤维细胞呈均匀弥散分布。本文还观察了细胞不同的周期时相和生长状态,以及不同的外界因素影响下 Con A 受体复合物的分布变异特点,并对 Con A 受体复合物在胃癌细胞质膜上不规则分布的原因进行了讨论。     

Concanavalin A receptors in the plasma membrane of rat liver cells: comparative electron microscopic studies on normal cells and on cells in vivo transformed by diethylnitrosamine.

The Concanavalin A receptors at the cell surface of normal rat liver cells and of those in vivo transformed by diethylnitrosamine were comparatively studied by electron microscopic cytochemistry. Besides different agglutinability of the cells a variable surface staining of the cells by the Con A-peroxidase reaction (BERNHARD and AVRAMEAS 1971) was observed. After performance of the cytochemical reaction on living normal rat liver cells in situ a continuous cell surface staining was seen. In transformed rat liver cells a marked tendency for patchy distribution of the Con A label at the cell surface occurred. Furthermore, internalisation of Con A-peroxidase labeled plasma membrane segments was visible in the transformed cells. A similar variable labeling by Con A-peroxidase reaction occured also in the "basal" plasma membrane of normal and transformed rat liver cells. The results are discussed with respect to the importance concerning the mobility of lectin receptors and membrane stability.     

Concanavalin A receptor sites on lymph node cells in vivo and in vitro

The distribution and density of receptors for concanavalin A (Con A) on the surfaces of cells of intact and isolated popliteal and axillary lymph nodes were investigated in the rabbit. Intact lymph nodes were perfused via the subcapsular (marginal) sinus with either Con A peroxidase or Con A ferritin, fixed with glutaraldehyde, and processed for electron microscopy. Both Con A peroxidase and Con A ferritin were distributed on the plasmalemma of lymphocytes, macrophages, neutrophils, plasma cells, reticular endothelial cells, and the vascular endothelium. Counts of Con A-conjugated ferritin particles indicated that the density of Con A receptors was generally similar for lymphocytes, macrophages, and neutrophils but lower on plasma cells. When lymph node cells were isolated by mechanical methods and exposed to Con A ferritin, the label was homogenously distributed on the cell surfaces of most cells. However, Con A binding was significantly higher on the surface of isolated cells than in the intact node. It is suggested that the increase in density of Con A binding sites on isolated cells may possibly be due to an unmasking of cell surface moieties in which additional Con A receptor sites become available as a result of the isolation procedure. The density of Con A ferritin binding sites was also significantly lower on the surface of isolated plasma cells than the lymphocyte and macrophage, suggesting that the density distribution of cell surface saccharides is different for various lymphoid cells.     

The behaviour of human ameloblastoma tissue in cell culture

Human ameloblastoma tissue was investigated using cell culture techniques, transmission electron microscopy and fluorescent microscopy. Cultured cellular morphology was dependent on the type of substratum, with polygonal cells predominant on collagen substrata in contrast to an elongated cellular morphology on glass substrata. The presence of tonofilaments and desmosomes confirmed the epithelial origin of these cells. The distribution of Con A surface receptors and cytoplasmic actin in the same cell was studied using a double fluorochrome technique. Incubation with fluorescein isothiocyanate-labelled Con A at 37°C for increasing time periods resulted in the Con A receptors showing progressive changes in staining patterns from clusters, to caps to perinuclear globules. Sequential changes in cytoplasmic actin, labelled by a specific anti-actin auto-antibody traced with rhodamine-labelled goat anti-human globulin, corresponded to the Con A staining patterns.     

Correlation between actin polymerization and surface receptor segregation in neuroblastoma cells treated with concanavalin A

Summary In response to concanavalin A (Con A), neuroblastoma cells undergo marked morphological changes which involve the retraction of neurites and the induction of broad and extensive lamellar regions around the cell periphery. From the use of FITC-Con A it was shown that the membrane formed on the induced lamellar regions lacked receptors to Con A from the onset of lamella formation. These receptors were confined to the cell body; they initially showed a uniform distribution and were subsequently collected into patches and finally into aggregates or caps. When the aggregates occurred on the cell periphery their position coincided with areas free of lamellae.Investigations of the lamellar regions in Triton-extracted cell monolayers showed them to consist of a meshwork of actin filaments containing radiating thin filament bundles or microspikes. With increasing time in the presence of Con A there was a progressive increase in the number of radiating microspikes. Previous studies have shown the actin in these lamellar regions to be singly polarized with respect to the cell body.From the segregation of Con A receptors away from areas of actin polymerization in the lamellae it is concluded that actin is involved in some indirect way in surface receptor movement.     

Location-specific regulation of transgenic Ly49A receptors by major histocompatibility complex class I molecules

Inhibitory receptors expressed on natural killer (NK) cells and T cells specific for major histocompatibility complex (MHC) class I are believed to prevent these cells from responding to normal self tissues. To understand the regulation and function of Ly49 receptor molecules in vivo, we used the CD2 promoter to target Ly49A expression to all thymocytes, T cells, and NK cells. In animals expressing its MHC class I ligand, H-2D^d or H-2D^k, there was a large decrease in the expression of Ly49A on thymocytes, peripheral T cells, and NK1.1⁺ cells. The extent of the down-regulation of Ly49A was dependent on the expression of the MHC ligand for Ly49A and on the site where the cells were located. The level of expression of endogenous Ly49A was similarly found to be dependent upon the organ where the cells resided. Data from bone marrow chimeras indicated that most cell types may regulate Ly49A expression, but the efficacy to regulate receptor expression may vary depending on the cell type.     

Age-related changes in natural killer cell receptors from childhood through old age

Most studies on natural killer (NK) cells and aging have focused on overall cell numbers and global cytotoxic activity. NK cell functions are controlled by surface receptors belonging to three major families: killer cell immunoglobulin-like receptors (KIRs), natural cytotoxicity receptors (NCRs), and C-type lectins. The expression of these receptors was investigated from childhood through old age in T, NKT- and NK cells and also in the CD56(dim) (cytotoxic) and CD56(bright) (responsible for cytokine production) NK cell subsets. A decrease in the expression of activating receptors (NKp30 and NKp46) was observed in NK cells in elderly individuals. KIR expression was increased only in the CD56(bright) subset. Children presented similar results regarding expression of NKp30 and KIR, but not NKp46. NKG2D expression was decreased in T cells of elderly subjects. Analysis of KIR genotype revealed that KIR2DL5 and KIR2DS3 were significantly associated with old age. Cytotoxic activity was preserved from childhood through old age, suggesting that the increase of the absolute number of CD56(dim), observed in elderly, may represent a compensatory mechanism for the receptor expression alterations. This initial study provides the framework for more focused studies of this subject, which are necessary to determine whether the changing balance of NK receptor expression may influence susceptibility to infectious, inflammatory, and neoplastic diseases.     

Quantifying the reduction in accessibility of the inhibitory NK cell receptor Ly49A caused by binding MHC class I proteins in cis

Murine natural killer (NK) cells are inhibited by target cell MHC class I molecules via Ly49 receptors. However, Ly49 receptors can be made inaccessible to target cell MHC class I by a cis interaction with its MHC class I ligand within the NK cell membrane. It has recently been demonstrated that MHC class I proteins transfer from the target cells to the NK cell. Here, we establish that the number of transferred MHC class I proteins is proportional to the number of Ly49A receptors at the NK cell surface. Ly49A+ NK cells from mice expressing the Ly49A ligand H-2D(d) showed a 90% reduction in Ly49A accessibility compared to Ly49A+ NK cells from H-2D(d)-negative mice. The reduction was caused both by lower expression of Ly49A and interactions in cis between Ly49A and H-2D(d) at the NK cell surface. Approximately 75% of the Ly49A receptors on H-2D(d)-expressing NK cells were occupied in cis with endogenous H-2D(d) and only 25% were free to interact with H-2D(d) molecules in trans. Thus, H-2D(d) ligands control Ly49A receptor accessibility through interactions both in cis and in trans.     

Expression of receptors for IgA on mitogen-stimulated human T lymphocytes

This study demonstrates that activation of human peripheral blood mononuclear cells (PBMC) by the T cell mitogens phytohemagglutinin (PHA) and concanavalin A (Con A) induces the expression of receptors for IgA without addition of IgA to the culture medium. Cells bearing receptors for IgA were determined by indirect immunofluorescence using human secretory IgA and fluoresceinated goat anti-human IgA or goat anti-secretory component antibodies. Among freshly isolated PBMC, 4.7 +/- 1.7% of T cells, 12.7 +/- 12.5% of B cells and 14.4 +/- 7.6% of monocytes were found to be IgA receptor positive. In unstimulated PBMC cultures the percentage of IgA receptor-positive cells slightly increased at 48 h and was more elevated after 7 days. In Con A-stimulated cultures 24.3 +/- 18.5% of the cells expressed receptors for IgA after 48 h. Then, the number decreased and rose again thereafter. PHA stimulation induced an increase of smaller magnitude with similar kinetics. Induction of receptor for IgA on activated T cells was demonstrated by double-labelling experiments showing more CD8+ than CD4+ cells with receptors for IgA among Con A-activated PBMC. Furthermore, PHA or Con A stimulation of B cell-depleted PBMC suspensions resulted in a marked increase of cells bearing receptors for IgA. Expression of these receptors was down-regulated by recombinant interferon-gamma (250 units/ml) and by prostaglandin PGE2 (100 nM) both on unstimulated and mitogen-activated PBMC. The receptor for IgA was distinct from the asialoglycoprotein receptor and did not cross-react with the poly-Ig receptor of epithelial cells. It was concluded that, in the absence of inducing exogenous IgA, T cell mitogens trigger the expression of receptors for IgA. Therefore, T cell activation is associated with the down-regulation of receptors for IgM and the increased expression of receptors for IgG, IgA and IgE.