黄芪在玉屏风散中的免疫调节作用及量效关系

本文观察了合不同剂量黄芪的玉屏风散对小鼠红细胞Ｃ３ｂ受体、粘附免疫复合物能力和血清中红细胞免疫调节因子的影响，结果表明黄芪以传统原方剂量配伍的玉屏风散能显著提高红细胞免疫功能，减少黄芪剂量作用降低，增加黄芪剂量也并不增强免疫功能，表明玉屏风散原方中黄芪剂量的合理性。     

艾灸对荷瘤小鼠免疫功能的影响

目的 :观察艾灸对荷瘤小鼠免疫功能的影响。方法 :将 40只荷瘤小鼠随机分为四组 ,对照组、艾灸组、5 氟脲嘧啶 ( 5FU)组、5FU +艾灸组。艾灸组、5FU +艾灸组分别在“中脘”、“神阙”、“关元”穴隔药饼灸 ,隔天 1次 ,治疗 8次。 5FU组、5FU +艾灸组在腹部注射 0 2 5mg/ 0 1mL5FU ,3天 1次 ,共治疗 4次。所有治疗完毕后 2 4hr处死动物。测定小鼠T淋巴细胞、自然杀伤细胞 (NK)及进行淋巴因子激活的杀伤细胞 (LAK)杀伤功能检测。结果 :艾灸组CD3、CD4、CD4/CD8比率、NK细胞、LAK杀伤活性比 5FU组显著提高 (P <0 0 5、P <0 0 0 5、P <0 1、P <0 1、P <0 0 1 ) ,差异明显 ,具有显著性意义。结论 :艾灸能提高小鼠的免疫力 ,而 5FU有抑制作用 ,使荷瘤小鼠免疫力降低     

Anti-idiotypic antibodies to anti-acetylcholinereceptor antibody: Characterization by ELISA and immunoprecipitation assays

The idiotype network is important both as a means of autoregulation of immune mechanisms and a potential tool for manipulation of abnormal responses. In the autoimmune disease myasthenia gravis the acetylcholine receptor (AChR) is the target of an aberrant immune response. In this study we compare 2 widely used methods of antibody determination--immunoprecipitation radioimmunoassay (IPRA) and enzyme-linked immunoassay (ELISA)--for their ability to detect both anti-AChR antibodies (polyclonal and monoclonal) and anti-idiotypic antibodies raised against polyclonal anti-AChR antibodies. Although the IPRA is considerably more sensitive for the detection of monoclonal anti-AChR antibodies, the 2 methods produce similar results in the detection of anti-idiotypic antibodies to the anti-AChR immune response. The 2 techniques also demonstrated specificity of the reagents for idiotypes associated with the anti-AChR response and absence of effect on an idiotype associated with the control antigen, ovalbumin. The results demonstrate that the idiotypic repertoire of the polyclonal anti-AChR response in C57B1/6 mice is sufficiently restricted that antigen-specific blocking anti-idiotypic antibodies can be raised in rabbits by immunization with anti-AChR antibodies.     

ConA诱导抑制细胞检测法的改进

ConA诱导抑制细胞检测应用于检测抑制性T细胞的功能状态。原法要采血二次,并经五天才能判断结果。本文采用同时培育刺激细胞和应答细胞的方法,仅需采血一次,且在三天后即可判断结果。     

Basic strategies of the immune system in the regulation of antibody response

Summary Three major regulatory mechanisms operating in the control of antibody response have been examined: 1. antibody feedback; 2. T cell regulation (I. regulatory interactions among T cell subsets, II. H-2 linked Ir gene control of T cell function, III. regulatory role of antigenic epitopes in T cell subsets induction); 3. idiotypic network. Analysis of the results obtained in the lysozyme system together with available data in the literature have permitted the delineation of a model of antigen-triggered events involved in the regulation of antibody response. The basic feature of the proposed model is the integration of two major specific communication systems among lymphocytes engaged in the antibody response: antigen bridge and idiotypic complementarity.     

风热清口服液对免疫低下小鼠免疫调节作用的研究

目的:探究风热清口服液对免疫低下小鼠免疫调节的作用。方法:通过给小鼠腹腔注射免疫抑制剂环磷酰胺50 mg/kg,1次/d,连续3 d,建立免疫功能低下的动物模型。应用碳廓清实验、溶血素生成实验和迟发型变态反应,评价风热清口服液对免疫低下小鼠非特异性免疫、体液免疫和细胞免疫的调节作用。结果:风热清口服液低、中剂量组可不同程度提高环磷酰胺致免疫低下小鼠的廓清指数K值(P<0.05)和吞噬指数α值(P<0.05)。风热清口服液低、中、高剂量组可不同程度提高免疫低下小鼠血清溶血素水平(P<0.05)。风热清口服液低、中剂量组可不同程度促进免疫低下小鼠迟发型变态反应(P<0.05)。风热清口服液低剂量组可提高免疫低下小鼠脾脏中CD4+细胞数(P<0.01),并使CD4+/CD8+细胞比值上升(P<0.001),同时抑制免疫低下小鼠脾脏中CD8+细胞数(P<0.05);风热清口服液中、高剂量组可提高免疫低下小鼠脾脏中CD4+/CD8+细胞比值(P<0.01),同时抑制免疫低下小鼠脾脏中CD8+细胞数(P<0.05)。风热清口服液低、中剂量组可显著提高免疫低下小鼠脾指数(P<0.001),风热清口服液低、中、高剂量组均可提高免疫低下小鼠胸腺指数(P<0.05或P<0.01)。结论:风热清口服液通过提高免疫低下小鼠非特异性免疫、体液免疫和细胞免疫,进而增强免疫低下小鼠的免疫功能。     

乙肝解毒汤对小鼠免疫功能的影响

目的：观察乙肝解毒汤对免疫功能的双向调节作用。方法：将50只小白鼠随机分为5组，每组10只，分别用硫唑嘌呤诱导免疫超常模型，用环磷酰胺诱导免疫低下模型。结果：乙肝解毒汤对免疫超常小白鼠的免疫功能有抑制作用；对免疫低下小白鼠的免疫功能有促进作用。结论：乙肝解毒汤对小白鼠的免疫功能有双向调节作用。     

Reduced IL-2 expression in NOD mice leads to a temporal increase in CD62Llo FoxP3+ CD4+ T cells with limited suppressor activity

IL-2 plays a critical role in the induction and maintenance of FoxP3-expressing regulatory T cells (FoxP3(+) Tregs). Reduced expression of IL-2 is linked to T-cell-mediated autoimmune diseases such as type 1 diabetes (T1D), in which an imbalance between FoxP3(+) Tregs and pathogenic T effectors exists. We investigated the contribution of IL-2 to dysregulation of FoxP3(+) Tregs by comparing wildtype NOD mice with animals congenic for a C57BL/6-derived disease-resistant Il2 allele and in which T-cell secretion of IL-2 is increased (NOD.B6Idd3). Although NOD mice exhibited a progressive decline in the frequency of CD62L(hi) FoxP3(+) Tregs due to an increase in CD62L(lo) FoxP3(+) Tregs, CD62L(hi) FoxP3(+) Tregs were maintained in the pancreatic lymph nodes and islets of NOD.B6Idd3 mice. Notably, the frequency of proliferating CD62L(hi) FoxP3(+) Tregs was elevated in the islets of NOD.B6Idd3 versus NOD mice. Increasing levels of IL-2 in vivo also resulted in larger numbers of CD62L(hi) FoxP3(+) Tregs in NOD mice. These results demonstrate that IL-2 influences the suppressor activity of the FoxP3(+) Tregs pool by regulating the balance between CD62L(lo) and CD62L(hi) FoxP3(+) Tregs. In NOD mice, reduced IL-2 expression leads to an increase in nonsuppressive CD62L(lo) FoxP3(+) Tregs, which in turn correlates with a pool of CD62L(hi) FoxP3(+) Tregs with limited proliferation.     

Regulatory T cells in viral hepatitis

The pathogenesis and outcome of viral infections are significantly influenced by the host immune response. The immune system is able to eliminate many viruses in the acute phase of infection. However, some viruses, like hepatitis C virus (HCV) and hepatitis B virus (HBV), can evade the host immune responses and establish a persistent infection. HCV and HBV persistence is caused by various mechanisms, like subversion of innate immune responses by viral factors, the emergence of T cell escape mutations, or T cell dysfunction and suppression. Recently, it has become evident that regulatory T cells may contribute to the pathogenesis and outcome of viral infections by suppressing antiviral immune responses. Indeed, the control of HCV and HBV specific immune responses mediated by regulatory T cells may be one mechanism that favors viral persistence, but it may also prevent the host from overwhelming T cell activity and liver damage. This review will focus on the role of regulatory T cells in viral hepatitis.