树突状细胞在支气管哮喘中的作用研究进展

支气管哮喘是由多种免疫细胞和炎性细胞因子参与发病的免疫系统性疾病。在支气管哮喘免疫过程发生的初始和维持阶段，树突状细胞对于过敏原的识别，摄取和提呈，CD4^＋T辅助细胞的分化和活化，以及气道变态反应和机体免疫耐受等方面发挥关键作用。通过干预树突状细胞在支气管哮喘发病机制中的作用，来达到治疗支气管哮喘的目的，已经成为目前指导临床用药的研究热点。     

树突状细胞在支气管哮喘中的作用研究进展

支气管哮喘是由多种免疫细胞和炎性细胞因子参与发病的免疫系统性疾病.在支气管哮喘免疫过程发生的初始和维持阶段,树突状细胞对于过敏原的识别,摄取和提呈,CD4+T辅助细胞的分化和活化,以及气道变态反应和机体免疫耐受等方面发挥关键作用.通过干预树突状细胞在支气管哮喘发病机制中的作用,来达到治疗支气管哮喘的目的,已经成为目前指导临床用药的研究热点.     

一氧化氮与支气管哮喘免疫学发病机制的关系

炎性细胞浸润和激活的细胞免疫应答在支气管哮喘(哮喘)发病机制中发挥重要作用。一氧化氮(NO)作为一种具有多种生物活性的气态生物信使,是多种免疫细胞的调节分子。近年有关NO在哮喘发病机制中的作用日渐受到重视,本文简述有关NO与免疫,尤其是与哮喘免疫炎性反应间关系的研究进展及临床意义。     

淋巴细胞凋亡在哮喘发病中的作用

目前有关支气管哮喘气道慢性炎症过程中淋巴细胞持续激活的主要环节及调控机制尚不十分清楚。免疫细胞尤其是淋巴细胞凋亡异常可能在哮喘气道慢性炎症的形成及发展中起重要作用。本文就淋巴细胞凋亡的调控及其在哮喘发病中的作用进行综述。     

一氧化氮与支气管哮喘免疫学发病机制的关系

炎性细胞浸润和激活的细胞免疫应答在支气管哮喘发病机制中发挥重要作用。一氧化氧（ＮＯ）作一种具有多处生物活性的气态生物信使，是多种免疫细胞的调节分子，近年有关ＮＯ在哮喘发病机制中的作用日渐受到重视，本简述有关ＮＯ与免疫，尤其是与哮喘免疫炎性反应间关系的研究进展及临床意义。     

支气管哮喘免疫调节治疗的研究进展

支气管哮喘(哮喘)是一种由多种免疫细胞及细胞组分参与的慢性气道炎症性疾病.随着对哮喘发病机制研究的不断深入,免疫调节治疗已成为哮喘研究中的一个新兴领域.本文对哮喘的免疫调节治疗方法新进展作一综述.     

粒细胞-巨噬细胞集落刺激因子与支气管哮喘的研究进展

粒细胞一巨噬细胞集落刺激因子(GM-CSF)可以由支气管哮喘(简称哮喘)炎症部位的巨噬细胞、嗜酸粒细胞和上皮细胞产生.反之,GM-CSF也同样作用于巨噬细胞、嗜酸粒细胞、免疫细胞、中性粒细胞等.GM-CSF的高表达增强了机体对抗原的敏感性,导致气道炎症反应增加,在哮喘发病机制中起着重要作用.     

粒细胞-巨噬细胞集落刺激因子与支气管哮喘的研究进展

粒细胞-巨噬细胞集落刺激因子（GM—CSF）可以由支气管哮喘（简称哮喘）炎症部位的巨噬细胞、嗜酸粒细胞和上皮细胞产生。反之,GM-CSF也同样作用于巨噬细胞、嗜酸粒细胞、免疫细胞、中性粒细胞等。GM—CSF的高表达增强了机体对抗原的敏感性,导致气道炎症反应增加,在哮喘发病机制中起着重要作用。     

哺乳动物壳多糖酶在支气管哮喘中的作用

壳多糖酶能够催化壳多糖中β(1→4)糖苷键的水解.近年来的研究发现,哺乳动物壳多糖酶可能在支气管哮喘发病中发挥着重要作用.对哺乳动物壳多糖酶在支气管哮喘发病中作用及机制的深入研究,有可能为支气管哮喘的治疗提供新的思路与方法.     

过敏性支气管哮喘免疫发病机制的最新研究进展

过敏性支气管哮喘(简称哮喘)是一种由不同的辅助性T细胞亚型决定的慢性气道炎症性疾病.既往认为“Th2哮喘假说”是过敏性哮喘的主要发病机制,而越来越多的研究表明,除了Th2之外其他辅助性T细胞也参与了哮喘的发病机制,尤其是Th1和Th17细胞对于气道中性粒细胞型炎症的发展至关重要.抑制这些免疫细胞也许为过敏性哮喘的有效治疗提供了方向.     

Distribution of immunoglobulin producing cells is different in normal human appendix and colon mucosa.

The densities of IgG-, IgA-, IgM- and IgD-producing immunocytes were determined by paired immunofluorescence staining and morphometric analysis in the lamina propria of normal appendix specimens. Normal colon specimens were used as reference material, mostly paired from individual subjects. The density (median of cells/mm2 lamina propria area) of IgA immunocytes tended to be slightly higher in the appendix than in the colon (1259 vs 962) and the same held true for IgM cells (71 vs 55). Conversely, the overall density of IgG immunocytes was much higher in the appendix than in the colon (95 vs 38). A striking feature was the fact that almost 50% of all immunocytes were of the IgG isotype adjacent to lymphoid follicles. It seemed justified to conclude, therefore, that the abundance of such follicles explains the overall enrichment of IgG-producing cells in normal appendix mucosa. These immunocytes most likely represent follicle derived B cells that have reached terminal maturation locally, whereas precursors generated from less mature memory clones probably emigrate and home ubiquitously to distant sites of the gut lamina propria where they develop into IgA-producing immunocytes.     

大鼠局灶性脑缺血再灌注后脑组织肾上腺髓质素的表达

目的 探讨肾上腺髓质素（adrenomedullin，ADM）在不同月龄大鼠脑缺血再灌注（I／R）脑组织的表达情况。方法 采用栓线法制成大鼠大脑中动脉I／R模型，阻断血流2h后再灌注4h。应用免疫组织化学染色法检测不同月龄段大鼠局灶性脑I／R后血浆ADM。结果 正常大鼠脑内即有ADM表达，假手术后ADM表达略有增加，但与正常对照组相比无明显差异（P〉0．05）；大鼠脑I／R后ADM免疫阳性细胞增多，与正常对照组及假手术组相比差异显著（均P〈0．05）；大鼠脑I/R后缺血侧及缺血对侧ADM免疫阳性细胞均增多，但以缺血侧区域增多最为明显（P〈0．05）。老龄大鼠脑I／R后ADM免疫阳性细胞数明显高于青年大鼠（P〈0．05）。结论 脑I／R后ADM表达增强，ADM表达增强与血管硬化相关。     

老龄大鼠慢性脑灌注不足与认知功能障碍的研究

目的　探讨老龄大鼠慢性脑灌注脑损害和认知功能障碍及其机制。方法　 5 0只老龄大鼠用于实验 ,其中 2 0只接受环孢菌素A(CsA)胃灌治疗。用光镜和电镜观察组织学改变 ,免疫组织化学法检测免疫细胞的活动 ,采用微机控制穿梭箱双向主动回避反应实验系统检测大鼠认知功能。结果　大鼠持久性双侧颈总动脉结扎 (2VO)诱导的慢性脑灌注不足造成了脑组织广泛免疫细胞活动和进行性脑损害 ,导致了大鼠进行性学习和记忆能力下降。CsA治疗组大鼠脑内免疫细胞的活动明显减少 ,脑损害明显减轻 ,学习和记忆能力显著提高。结论　脑组织免疫细胞的活动贯穿于大鼠慢性脑灌注不足脑损害的病理过程 ,在脑损害和认知功能障碍的发生和发展中起重要作用 ;CsA可明显减轻脑内免疫细胞的活动 ,防治了大鼠的脑损害和认知功能障碍。     

Mucosal subclass distribution of immunoglobulin G-producing cells is different in ulcerative colitis and Crohn's disease of the colon

As a marked local immunoglobulin G (IgG) response has previously been found to be the most prominent immunopathological feature of both ulcerative colitis and Crohn's disease, the subclass distribution of colonic IgG-producing immunocytes was examined. This study included tissue specimens from 10 patients with ulcerative colitis and 8 with Crohn's colitis. Paired immunofluorescence staining was performed with subclass-specific murine monoclonal antibodies combined with a rabbit antibody reagent of IgG; the proportion of cells belonging to each subclass could thereby be determined in relation to the total number of mucosal IgG immunocytes. A significantly higher median proportion of IgG1 immunocytes was found in ulcerative colitis (81.3%) than in Crohn's colitis (66.5%). Conversely, the median proportion of IgG2 immunocytes was significantly higher in Crohn's colitis (24.9%) than in ulcerative colitis (9.4%). This disparity in the local IgG subclass response might reflect dissimilar mucosal exposure to mitogenetic or antigenic stimuli or genetically determined immunoregulatory differences in the two categories of patients.     

Studies of the immunoglobulin-producing cells of the human intestine: the defunctioned bowel.

An indirect immunoperoxidase method was used to visualise immunoglobulin-containing cells in the large intestinal mucosa of 10 children who had defunctioning colostomies. Intestine deprived of its usual exposure to intraluminal antigens contained less immunocytes per unit area than intestinal mucosa subjected to normal stimulation by dietary and microbial antigens. These findings substantiate in man the conclusion based on observations made on animals that continued mucosal exposure to antigenic stimulation is necessary for the existence of an adequate population of intestinal immunocytes.     

Effect of alcohol-feeding on IgA-producing immunocytes in the small intestine of rats with and without jejunoileal bypass

Alcohol-feeding to rats subjected to jejunoileal bypass operation has been shown to lead to marked liver injury (fatty liver, necrosis and inflammation). This study investigated the influence of alcohol-feeding over a period of 3 months on the number of IgA-producing immunocytes and the villus surface area in various sections of the small intestine of rats subjected to a jejunoileal bypass or a sham operation. A jejunoileal bypass in animals receiving the control diet led to a decrease in the number of IgA-producing immunocytes in the duodenum and ileum, but not in the bypassed (blind) loop of the jejunum. In animals subjected to a jejunoileal bypass, alcohol-feeding led to an increase in the number of IgA-producing immunocytes in the duodenum and the bypassed jejunal loop as compared with animals with a jejunoileal bypass receiving the control diet. Among the animals with a jejunoileal bypass fed the control diet, the villus surface area within the duodenum and ileum increased as compared with the groups of sham-operated rats. The feeding of alcohol prevented this increase in the villus surface area in animals with a jejunoileal bypass. The increase in the number of IgA-producing immunocytes induced by alcohol in the animals with a jejunoileal bypass, in the duodenum and bypassed jejunum, supports the assumption of a change in antigen uptake in these parts of the small intestine, brought about by alcohol.     

老年患者恶性胸水中肿瘤浸润免疫细胞体外活化

目的 观察老年患者恶性胸水中肿瘤浸润免疫细胞的活性.方法 分离恶性胸水单个核细胞(PEMCs),采用两步贴壁法,获得非贴壁细胞,树突细胞及淋巴细胞是其主要功能细胞成分.IL-2活化肿瘤浸润免疫细胞,SP法检测T淋巴细胞亚群的数量及免疫功能,SP法S-100蛋白染色检测树突细胞.结果 IL-2活化培养7 d后肿瘤浸润树突细胞(TIDC)和肿瘤浸润T淋巴细胞(TIL)数量明显增加(P<0.01).恶性胸水TIDC经过IL-2活化后具有抗原提呈功能.结论 IL-2活化肿瘤微环境中TIDC,使其恢复免疫监视功能,有效地负载肿瘤抗原,协同TIL等其他免疫细胞有效杀伤肿瘤细胞.     

Light microscopic morphometric analysis of rat ileal mucosa

A light microscopic morphometric analysis of IgA-containing immunocytes within samples of ileal mucosa was performed. The following groups of rats were studied: (1) animals raised in a gnotobiotic environment (microbial reduction); (2) animals with iatrogenic self-filling intestinal blind loops (microbial proliferation); and (3) control animals (sham operation). The unlabeled antibody enzyme immunohistochemical localization technique was employed for the identification of intracellular IgA. Component quantitation involved use of a micrometer component quantitator. Numerical density of the immunocyte population was determined by component quantitation of individual and total immunocyte volumes and by application of the Floderus equation. The methodology employed provided a precise quantitative analysis of all mucosal components of normal and manipulated rat ileum. A statistically significant reduction in the volume percentage of IgA-containing immunocytes in association with both microbial reduction and microbial proliferation was observed. The volume percentage reduction of the IgA-containing immunocyte population associated with gnotobiosis may reflect decreased microbial antigenic stimulation, whereas that associated with microbial proliferation may reflect the presence of an increased population of immunocytes producing non-IgA immunoglobulins.     

Autacoids as modulators of the inflammatory and immune response

Once considered only mediators of inflammation, autacoids, (histamine, prostaglandins and beta-mimetic catecholamines) have been found to be generated during specific early and late phases of immunity. They need sufficient concentrations to affect immunocytes and can modulate immunity usually by inhibiting it. Receptors for the autacoids on the immunocytes are nonrandomly distributed. A small portion of T suppressor cells always appear to have receptors on them, but precursor B cells and precursors of T cells that produce lymphokines or are responsible for cytolysis do not. Instead, as these cells mature they develop their autacoid receptors. With one exception, the function of the immunocytes is inhibited by the effects of autacoids. Again, in all but one instance, that inhibitory modulating effect is mediated by and directly proportional to the intracellular concentrations of cyclic adenosine monophosphate (AMP) generated by the autacoid. The clinical implications of these observations are beginning to be appreciated. One of them is that pharmacologic antagonists of the autacoids can have predictable but hitherto unanticipated effects on immune functions. It is inconceivable that these effects will not have clinical value.     

Mast cells and immunoglobulin E in inflammatory bowel disease.

The numbers of mast cells and of IgE-containing immunocytes in the bowel wall of patients suffering from Crohn's disease of ulcerative colitis have been estimated and the results compared with those found in normal control specimens. In ulcerative colitis there is a slight rise in the number of mast cells and it appears that these participate in the inflammatory process in a non-specific manner; the number of IgE-containing immunocytes is not significantly altered. In Crohn's disease there is an almost total absence of stainable mast cells in affected areas of the bowel, together with a marked decrease in IgE-containing immunocytes. It is suggested that these findings are due to degranulation of mast cells and consumption of IgE as a result of an immediate hypersensitivity reaction in the bowel wall, this being one component of the protein inflammatory and immunological response to the entry of a variety of antigenic material.