甘氨胆酸对小鼠体外脾淋巴细胞凋亡的影响

本研究旨在探索不同浓度的甘氨胆酸(Glycocholic acid,GCA)对小鼠体外脾淋巴细胞凋亡的影响。在0.02μg/ml,0.035μg/ml,0.07μg/ml,0.21μg/ml,1.05μg/mL不同浓度的GCA作用下,应用倒置显微镜观察了体外脾淋巴细胞的核形态,采用琼脂糖凝胶电泳法检测了脾淋巴细胞的DNA片段,采用流式细胞仪测定了脾淋巴细胞凋亡早期磷脂酰丝氨酸外翻百分率;采用分光光度法测定了凋亡细胞氧化还原反应活性——GSH的含量;通过ELISA法检测了Caspase-3和Caspase-9的活性。结果:GCA能够使脾淋巴细胞细胞产生核固缩和凋亡小体;显著引起脾淋巴细胞DNA片段化(P<0.05),极显著的诱导脾淋巴细胞磷脂酰丝氨酸外翻(P<0.01);显著降低GSH的含量(P<0.05);显著提高Caspase-9和Caspase-3的活性(P<0.05)。结论:GCA具有显著的提高小鼠体外脾淋巴细胞凋亡的作用(P<0.05)。     

绵羊肺腺瘤病毒人工感染羊重要病理生理指标的检测

进一步探讨人工感染绵羊肺腺瘤病毒的羊对淋巴细胞亚群、淋巴细胞凋亡、血气指标、肿瘤标志物的影响.对已人工感染JSRV 300d的病羊,进行临床指标测定,每隔30d用流式细胞仪检测外周血中淋巴细胞及其亚群的动态变化以及淋巴细胞凋亡情况.同时,对血液做血气分析、血清酶和肿瘤标志物的检测.结果:SPA攻毒组感染JS-RV - ...     

Lymphocyte stimulation: transfer of cellular hypersensitivity to antigen in vitro

Tuberculin-sensitive human lymphocytes cultured for 36 hours with tuberculin elaborate a soluble material which causes nonsensitive lymphocytes to respond to tuberculin in vitro by transformation and proliferation.     

Rat thoracic duct lymphocytes: types that participate in inflammation

Newly formed small lymphocytes with a short life-span in the blood are the only cells from thoracic duct lymph which accumulate in acutely inflamed tissue. This conclusion is drawn from studies in which rats with induced peritonieal exudates were injected intravenously with radioactively labeled thoracic duct cells. Radioactivity, originally vested in newly formed donor small lymphocytes, was found later in a small number of similar exudate cells. Small lymphocytes generated 10 days or more before the thoracic ducts were cannulated failed to localize in peritoneal exudates, although the cells moved in large numbers from the blood in to lymph nodes.     

棉酚对多浪羊淋巴细胞凋亡的影响

通过棉酚对多浪羊淋巴细胞的研究,探索棉酚体积分数对淋巴细胞的影响.主要用细胞培养、瑞氏-吉姆萨染色、DNA电泳等方法观察棉酚对多浪羊淋巴细胞的凋亡效应.结果表明:当细胞培养液中棉酚体积分数为0.071mol/L,培养淋巴细胞8h后,可抑制多浪羊淋巴细胞的增殖,并且促进其凋亡.     

鸡外周血淋巴细胞培养及转移因子的提取

转移因子(TransferFactor,简称TF)是白细胞中具有免疫活性的T淋巴细胞所释放的一类小分子可透析物质。在传统转移因子制备方法的基础上,采用鸡外周血淋巴细胞培养法研制转移因子,并对制备转移因子中的核糖含量进行测定。结果表明:连续传代4次的淋巴细胞可以提取转移因子,转移因子的浓度较高。     

Antibody-dependent lymphoid cell-mediated cytotoxicity: no requirement for thymus-derived lymphocytes

The capacity of lymphoid cells from nonsensitized mice to lyse antibody-coated target erythrocytes in vitro does not require the presence of thymus-derived or thymus-dependent lymphocytes. Thus, spleen cells from thymus-deprived mice and spleen cell populations from which thymus-dependent lymphocytes had been removed were fully competent to mediate destruction of antibody-coated target cells. However, prior treatment of spleen cell populations with antibody to kappa chains diminished this function, suggesting a role for bone marrow-derived lymphocytes.     

Autosensitization of lymphocytes against thymus reticulum cells

Lymph nodes of normal rats contain lymphocytes that can be induced in vitro to mediate a specific cellular immune reaction against reticulum cells derived from syngeneic adult thymus glands. It is likely that these lymphocytes had access to reticulum cell antigens during the period in which they developed immunocompetence within the thymus. This suggests that contact with self-antigens during development may not eliminate self-reactive lymphocytes. These findings are in conflict with the theory that natural tolerance to self-antigens depends upon elimination of lymphocyte clones.     

Involvement of sialic acid on endothelial cells in organ-specific lymphocyte recirculation

Mouse lymphocytes incubated on cryostat-cut sections of lymphoid organs (lymph nodes and Peyer's patches) specifically adhere to the endothelium of high endothelial venules (HEV), the specialized blood vessels to which recirculating lymphocytes attach as they migrate from the blood into the parenchyma of the lymphoid organs. Treatment of sections with sialidase eliminated the binding of lymphocytes to peripheral lymph node HEV, had no effect on binding to Peyer's patch HEV, and had an intermediate effect on mesenteric lymph node HEV. These results suggest that sialic acid on endothelial cells may be an organ-specific recognition determinant for lymphocyte attachment.     

外泌体及其miR-155参与免疫细胞之间的通讯

外泌体是一种细胞分泌的囊泡，里面含有丰富的核酸和蛋白质等物质，对于信息的传递、免疫功能的调节具有重要作用.本研究通过培养巨噬细胞、树突状细胞，收集上清液，分别采用外泌体提取试剂盒法和超速离心法提取外泌体，使用透射电镜法和Western blot法进行外泌体鉴定. 将提取的外泌体转染荧光标记，与淋巴细胞共同孵育24 h.采用含荧光标记的miR-155，分别转染到巨噬细胞和树突细胞中，提取细胞上清的外泌体，与淋巴细胞共孵育24 h.结果显示：超速离心法提取的外泌体更纯，但是SBI试剂盒提取的外泌体更多，适用于下一步试验；巨噬细胞及树突状细胞分泌的外泌体加荧光标记与淋巴细胞共培养后，可使淋巴细胞荧光增加；荧光标记miR-155的外泌体与淋巴细胞共培养，可使淋巴细胞荧光增加. 本研究证实了树突细胞、巨噬细胞分泌的外泌体及其包含的miR-155可作用于淋巴细胞，参与免疫细胞间的通讯，为进一步阐明外泌体的作用机制奠定了理论基础.     

Prevention of type I diabetes in nonobese diabetic mice by virus infection

The nonobese diabetic (NOD) mouse is an animal model of type I diabetes and develops a characteristic autoimmune lesion in the islets of Langerhans with lymphocytic infiltration and destruction of pancreatic beta cells. The result is hypoinsulinemia, hyperglycemia, ketoacidosis, and death. Diabetes usually begins by the sixth month of age but can occur earlier when young NOD mice are infused with lymphocytes from older NOD donors. When newborn or adult NOD mice were infected with a lymphotropic virus they did not become diabetic. The interaction between viruses and lymphocytes is pivotal in aborting diabetes, as established by experiments in which lymphocytes from virus-infected donors failed to transfer diabetes. In contrast, lymphocytes from age- and sex-matched uninfected donors caused disease. Therefore, viruses and, presumably, their products can be developed to be beneficial and may have potential as a component for treatment of human diseases. Further, these results point to the utility of viruses as probes for dissecting the pathogenesis of a nonviral disease.     

不同泌乳阶段和产奶水平对奶牛淋巴细胞凋亡的影响

选择48头奶牛,分为6组,每组8头,分别为泌乳盛期,泌乳中期和泌乳末期,每个泌乳期设高产组和低产组,研究不同泌乳阶段和产奶水平下奶牛外周血淋巴细胞凋亡情况。结果表明:随着泌乳阶段的延长淋巴细胞凋亡率显著升高,其中泌乳末期最高为2.95%,显著高于泌乳盛期(P0.05),泌乳中期淋巴细胞凋亡和各阶段差异不显著;在泌乳盛期和泌乳中期,高产奶牛的外周血淋巴细胞凋亡率极显著地高于低产奶牛(P0.01),泌乳末期低产组淋巴细胞凋亡率升高为3.02%,高产组低产组,但差异不显著(P0.05)。由此可见,随着泌乳时间的延长,奶牛外周血淋巴细胞的凋亡率逐渐上升,并且高产奶牛更易于发生淋巴细胞的凋亡。     

A distinct endothelial cell recognition system that controls lymphocyte traffic into inflamed synovium

Lymphocytes are essential mediators of normal tissue inflammatory reactions and of pathologic tissue damage in, for example, rheumatoid arthritis and other autoimmune diseases. In a study of the mechanisms controlling lymphocyte entry into sites of inflammation from the blood, the function and specificity of lymphocyte-endothelial interactions were examined in inflamed joint tissue (synovium) from patients with rheumatoid arthritis. Synovial high endothelial venules (HEV) supported the binding of normal peripheral blood lymphocytes in vitro. The characteristics of this binding, which were similar to those of lymphocyte-HEV interactions controlling lymphocyte migration into organized lymphoid tissues, included a requirement for calcium ions, a dependence on metabolic activity, and a preferential adherence of circulating lymphocytes as opposed to immature thymocytes. However, the binding of lymphocytes to synovial HEV was not inhibited by a monoclonal antibody to lymphocyte receptors for lymph node HEV, and synovial HEV failed to bind either lymph node HEV-specific or mucosal HEV-specific B lymphoblastoid cells. The results suggest that a lymphocyte-endothelial cell recognition system that is distinct from such systems in organized lymphoid tissues directs the extravasation of normal lymphocytes as well as pathologically important effector cells into inflamed synovium.     

Mycoplasma inhibition of phytohemagglutinin stimulation of lymphocytes

Goat lymphocytes were cultured in vitro with phytohemagglutinin and nonviable mycoplasmas. Addition of the mycoplasmas, even as late as 45 hours after adding phytohemagglutinin, completely inhibited the increase in synthesis of DNA and RNA normally induced in lymphocytes by the mitogen. The suppression of synthesis did not result from killing of the cells by the mycoplasmas, combination of the organisms with phytohemagglutinin, or competition for combining sites on the cell surface, which indicates that some other mechanism of inhibition was operative. A similar depression of response to phytohemagglutinin in lymphocytes in culture has been observed in human diseases associated with an immune defect. The present demonstration that at least certain mycoplasmas can profoundly affect lymphocyte function in vitro suggests that thay may alter the immune response in vivo.     

REV与ALV-J共感染对肉鸡T淋巴细胞免疫功能与组织病理学的影响

 【目的】研究致瘤性病毒REV、ALV-J单一感染和共感染肉鸡后血液和脾T淋巴细胞的免疫功能与脾组织病理学的变化。【方法】用一定剂量的REV和ALV-J单一感染及共感染1日龄肉鸡,取感染后不同日龄鸡的血液和脾组织,无菌分离淋巴细胞,用3H-TdR掺入法和MTT法分别检测T淋巴细胞增殖活性和细胞毒T淋巴细胞(CTL)的杀伤活性,并对脾脏进行组织切片、H.E染色检测组织病理学变化,通过免疫荧光抗体结合试验(immunofluorescence assay,IFA)分析组织病毒感染量变化。【结果】感染REV和ALV-J的肉鸡血液和脾T淋巴细胞的增值活性和CTL杀伤活性在整个感染监测期出现降低,单一感染比,共感染两种病毒的肉鸡在某些阶段出现T淋巴细胞免疫功能抑制加重;检测感染后17 d和37 d的脾脏组织病理学变化表明感染病毒的脾脏组织出现间质稀疏,淋巴细胞数量减少,生发层被破坏或减少,17 d较37 d出现病理变化更为明显;同时采用荧光标记的单克隆抗体进行IFA检测发现脾内淋巴细胞含有大量病毒粒子,在共感染两种病毒的肉鸡脾细胞内均检测出两种病毒,且含有病毒数量明显多于单一感染一种病毒的肉鸡。【结论】REV和ALV-J共感染后肉鸡T淋巴细胞功能抑制更为严重,这可能与两种病毒在肉鸡体内数量积聚增加、互为促进有重要关系;同时这两种病毒感染后造成T免疫细胞增殖活性和对肿瘤细胞的杀伤活性降低,可能是病毒持续感染、增殖及组织病变、产生肿瘤细胞的前提,本研究为家禽临床生产中防治REV和ALV-J感染提供免疫学基础。     

马蹄香含药血清对小鼠脾淋巴细胞和腹腔巨嗜细胞的影响

[目的]研究马蹄香（Valeriana jatamansiJones）含药血清对小鼠脾淋巴细胞及腹腔巨嗜细胞的影响。[方法]通过MTT法检测含药血清对正常小鼠脾淋巴细胞转化的影响,结合中性红吞噬实验检测含药血清对小鼠腹腔巨噬细胞能量代谢水平及吞噬能力的影响。[结果]在一定剂量范围内,马蹄香含药血清组的脾淋巴细胞和腹腔巨噬细胞无论单独作用或协同非特异性丝裂原（Con A或LPS）作用与对照组均有显著性差异。[结论]马蹄香含药血清能够增强小鼠脾淋巴细胞转化能力,提高腹腔巨噬细胞能量代谢水平和吞噬能力,具有一定的免疫增强作用。     

Autoimmune encephalomyelitis: activation of thymus lymphocytes against syngeneic brain antigens in vitro

Thymus lymphocytes of normal adult rats were autosensitized in vitro against soluble antigens extracted from the brains of syngeneic rats. Injection of the autosensitized lymphocytes into syngeneic rats led to the development of brain lesions suggestive of autoimmune encephalomyelitis. Injection of control lymphocytes or the antigen extract alone did not cause lesions. Since sensitization in vitro requires the presence of lymphocytes programmed with specific receptors, the results indicate that normal rats have lymphocytes capable of recognizing central nervous system self-antigens. Hence, regulatory mechanisms, inoperative in vitro, probably function in vivo to prevent immune activation of self-recognizing lymphocytes and autoimmunity. This concept suggests a new approach to exploring the pathogenesis of autoimmune diseases.     

Increased sensitivity of lymphocytes from people over 65 to cell cycle arrest and chromosomal damage

Flow cytometry revealed that, in the presence of tritiated thymidine, a greater percentage of phytohemagglutinin-stimulated lymphocytes from old human donors were arrested in the G2 or M phase than were cells from young donors. Furthermore, lymphocytes from old donors showed significantly more chromosomal damage than did lymphocytes from young donors. Lymphocyte cultures from old or young donors not exposed to tritiated thymidine had the same percentage of cycling lymphocytes in G2 or M, although the number of lymphocytes stimulated by phytohemagglutinin to enter the cell cycle was significantly lower in cultures from old donors. Thus, the impaired incorporation of tritiated thymidine by phytohemagglutinin-exposed lymphocytes from old humans reflects both an impaired proliferative response to phytohemagglutinin and an increased sensitivity to the radiobiological effects of tritiated thymidine.     

Cytotoxic action of stimulated lymphocytes on allogenic and autologous erythrocytes

Fowl erythrocytes are lysed when exposed to an excess of fowl blood lymphocytes in the presence of phytohemagglutinin. No significant cell damage is seen in the absence of phytohemagglutinin, or when the lymphocytes are replaced by malignant lymphoid cells, thymus cells, or nonlymphoid cells. The lymphocytes remain viable during the reaction. Differences in histocompatibility between lymphocytes and erythrocytes are not required. Autologous lymphocytes are cytotoxic to the same extent as allogenic lymphocytes over a wide range of experimental conditions.