甲壳动物细胞及体液免疫机理的研究进展

根据国内外的有关资料,对甲壳动物细胞及全液免疫进行了简要的评述，其机体的免疫防御功能主要依赖于血细胞的吞噬，包掩等细胞免疫反应，但目前对于血细胞的分类及各自的功能尚无定论，甲壳动物体液吵具有免疫球蛋白，缺乏抗体介导的免疫反应，其体液免疫主要是指血淋巴中的一些酶和调节因子，如酚氧化酶原激活系统，落血素，凝集素，溶菌酶，蛋白酶抑制剂等。     

检疫中生猪淋巴结病变及其重要性

<正>淋巴结是猪宰后检疫的一个重要指标。淋巴结具有产生淋巴细胞、浆细胞及单核细胞的造血机能,并与机体的免疫功能密切相关,是机体外周的免疫器官和防御结构,具有吞噬异物和各种微生物的功能,并产生免疫应答。当机体某组织或器官受到病原微生物侵害时,很快被局部淋巴结阻     

中华绒螯蟹的免疫学研究现状与前景展望

中华绒螯蟹免疫学的研究进展表明其机体的免疫防御机能主要依靠血细胞的吞噬、包掩等细胞免疫反应;中华绒螯蟹与其它的甲壳动物一样,体液中不具有免疫球蛋白,缺乏抗体介导的免疫反应,其体液免疫主体是血淋巴中的一些酶(如溶菌酶、酚氧化酶、超氧化物歧化酶等)、免疫因子(如凝集素、溶血素等)以及调节因子如酚氧化酶原激活系统等;并期望加强河蟹基础免疫的研究,为其免疫预防提供理论依据。     

中华绒螯蟹的免疫学研究现状与前景展望

中华绒螯蟹免疫学的研究进展表明其机体的免疫防御机能主要依靠血细胞的吞噬、包掩等细胞免疫反应;中华绒螯蟹与其它的甲壳动物一样,体液中不具有免疫球蛋白,缺乏抗体介导的免疫反应,其体液免疫主体是血淋巴中的一些酶(如溶菌酶、酚氧化酶、超氧化物歧化酶等)、免疫因子(如凝集素、溶血素等)以及调节因子如酚氧化酶原激活系统等;并期望加强河蟹基础免疫的研究,为其免疫预防提供理论依据。     

异育银鲫对嗜水气单胞菌灭活菌苗的免疫应答

采用神尔马林灭活的嗜水气单胞菌（Aeromondas hydrophila)菌苗免疫接种异育银鲫，通过测定受免鱼血清中凝集抗体效价，溶菌酶活性，血液中吞噬细胞的吞噬活性，杀菌活性并通过鱼体攻毒试验，探讨了异育银鲫对福尔马林灭活的嗜水气单胞菌菌苗的免疫应答状况，结果表明，接种28d后，受免鱼血清中凝集抗体效价和溶菌酶活性均值分别为1：18.89和156.36U/dml，相应的对照组则为1：0.83和138.68dU/ml；受免鱼血中白细胞吞噬百分比和吞噬指数分别为63.38%和6.02，而对照组的分别库存47.95%和5.08；免疫组和对照组白细胞的杀菌指数分别为1.59和1.15，受免鱼的免疫保护力达到73.7%。     

α-甘露聚糖肽对鲫鱼免疫应答强度的影响研究

为研究α-甘露聚糖肽(M annatide)对鲫鱼免疫应答强度的影响,将α-甘露聚糖肽按每天每千克体重1.5 m g的剂量拌饵投喂鲫鱼,分别于7,14,21和28 d时检测各组鲫鱼吞噬细胞的杀菌活性、白细胞的吞噬活性、SOD酶活性和血清凝集抗体效价。结果表明,不同投喂周期均可增强鲫鱼的免疫应答强度;用药饵投喂7 d的试验组,7 d后免疫应答强度很快与对照组趋于一致;21 d和28 d投喂组的免疫应答强度差异不明显,但均显著(P<0.05)高于14 d组。因此,投喂21 d左右即可达到使非特异性免疫功能增强持续30 d以上的效果。     

功能性饵料添加剂对水产动物免疫机能的影响

许多营养性和非营养性饵料添加剂如中草药活性成分(多糖、生物碱、皂甙、有机酸等)、寡聚糖、维生素、微量元素等对水产动物机体的免疫机能都有不同程度的调节作用,适当使用这些功能性添加剂能够提高其自身的免疫功能特别是非特异性免疫功能,如提高吞噬细胞的数量及其吞噬功能,溶菌酶活性以及其他一些免疫因子如补体、干扰素、溶血素的释放等。     

温度对虾蟹生长发育影响的研究进展

虾、蟹等甲壳动物作为变温动物,环境温度(特别是水温)的变化对其健康状况、生理机能(包括存活、生长、生殖和免疫应答等)及行为影响很大。本文总结温度对虾蟹生长发育、免疫和生殖等方面影响的研究进展,以期为今后的相关研究提供参考。     

虫草多糖对日本沼虾免疫机能的影响

在饲料中添加1‰的虫草多糖，以口服形式对日本沼虾进行免疫，通过连续测定日本沼虾血淋巴吞噬活性，血清中抗菌活力、溶菌活力以及酚氧化酶活力，研究虫草多糖对日本沼虾免疫机能的作用，结果表明：除个别情况外，虫草组的吞噬百分比和吞噬指数、抗菌活力、溶菌活力以及酚氧化酶活力、均高于对照组，因此，投喂虫草多糖能够明显地增强日本沼虾的免疫防御能力。     

硬骨鱼补体系统的研究进展

综述了各种硬骨鱼物种具体的补体成分的特点,以及鱼类补体在调理、吞噬、免疫应答、炎症介导及病原体的防御和清除中的作用,并从生理角度评估了影响补体活性水平及其组分的因子,此外,笔者还提出了一些硬骨鱼补体系统未来的研究方向。     

Toll-like receptor signaling pathways

Members of the Toll-like receptor (TLR) family recognize conserved microbial structures, such as bacterial lipopolysaccharide and viral double-stranded RNA, and activate signaling pathways that result in immune responses against microbial infections. All TLRs activate MyD88-dependent pathways to induce a core set of stereotyped responses, such as inflammation. However, individual TLRs can also induce immune responses that are tailored to a given microbial infection. Thus, these receptors are involved in both innate and adaptive immune responses. The mechanisms and components of these varied responses are only partly understood. Given the importance of TLRs in host defense, dissection of the pathways they activate has become an important emerging research focus. TLRs and their pathways are numerous; Science's Signal Transduction Knowledge Environment's TLR Connections Map provides an immediate, clear overview of the known components and relations of this complex system.     

Induction of protective IgA by intestinal dendritic cells carrying commensal bacteria

The enormous number of commensal bacteria in the lower intestine of vertebrates share abundant molecular patterns used for innate immune recognition of pathogenic bacteria. We show that, even though commensals are rapidly killed by macrophages, intestinal dendritic cells (DCs) can retain small numbers of live commensals for several days. This allows DCs to selectively induce IgA, which helps protect against mucosal penetration by commensals. The commensal-loaded DCs are restricted to the mucosal immune compartment by the mesenteric lymph nodes, which ensures that immune responses to commensal bacteria are induced locally, without potentially damaging systemic immune responses.     

Regulation of homeostatic chemokine expression and cell trafficking during immune responses

The chemokines CCL21 and CXCL13 are immune factors that dictate homing and motility of lymphocytes and dendritic cells in lymphoid tissues. However, the means by which these chemokines are regulated and how they influence cell trafficking during immune responses remain unclear. We show that CCL21 and CXCL13 are transiently down-regulated within lymphoid tissues during immune responses by a mechanism controlled by the cytokine interferon-gamma. This modulation was found to alter the localization of lymphocytes and dendritic cells within responding lymphoid tissues. As a consequence, priming of T cell responses to a second distinct pathogen after chemokine modulation became impaired. We propose that this transient chemokine modulation may help orchestrate local cellularity, thus minimizing competition for space and resources in activated lymphoid tissues.     

Innate immunity in Caenorhabditis elegans is regulated by neurons expressing NPR-1/GPCR

A large body of evidence indicates that metazoan innate immunity is regulated by the nervous system, but the mechanisms involved in the process and the biological importance of such control remain unclear. We show that a neural circuit involving npr-1, which encodes a G protein-coupled receptor (GPCR) related to mammalian neuropeptide Y receptors, functions to suppress innate immune responses. The immune inhibitory function requires a guanosine 3',5'-monophosphate-gated ion channel encoded by tax-2 and tax-4 as well as the soluble guanylate cyclase GCY-35. Furthermore, we show that npr-1- and gcy-35-expressing sensory neurons actively suppress immune responses of nonneuronal tissues. A full-genome microarray analysis on animals with altered neural function due to mutation in npr-1 shows an enrichment in genes that are markers of innate immune responses, including those regulated by a conserved PMK-1/p38 mitogen-activated protein kinase signaling pathway. These results present evidence that neurons directly control innate immunity in C. elegans, suggesting that GPCRs may participate in neural circuits that receive inputs from either pathogens or infected sites and integrate them to coordinate appropriate immune responses.     

Cancer immunotherapy: a treatment for the masses

Cancer immunotherapy attempts to harness the exquisite power and specificity of the immune system for the treatment of malignancy. Although cancer cells are less immunogenic than pathogens, the immune system is clearly capable of recognizing and eliminating tumor cells. However, tumors frequently interfere with the development and function of immune responses. Thus, the challenge for immunotherapy is to use advances in cellular and molecular immunology to develop strategies that effectively and safely augment antitumor responses.     

金黄色葡萄菌5型荚膜多糖偶联鞭毛蛋白疫苗对小鼠乳腺炎模型的保护作用

[目的]金黄色葡萄菌5型荚膜多糖(CP5)分别与鼠伤寒沙门氏菌鞭毛蛋白Flagellin、牛血清白蛋白(BSA)进行了偶联,并在小鼠模型上比较了这2种偶联疫苗所引起的体液免疫和粘膜免疫反应。[方法]以鼠伤寒沙门氏菌鞭毛蛋白为载体蛋白,与CP5进行化学偶联,并在小鼠乳腺部位免疫,然后通过检测小鼠乳汁中的抗体分析其对小鼠的免疫保护作用。[结果]乳腺局部免疫后flagellin-CP5组在乳腺部位引起了sIgA为代表的粘膜免疫反应和IgG为主的体液免疫反应。CP5和鞭毛蛋白的偶联物能够诱导更高的体液免疫以及粘膜免疫反应。[结论]鞭毛蛋白具有较强的免疫佐剂作用。     

Direct ubiquitination of pattern recognition receptor FLS2 attenuates plant innate immunity

Innate immune responses are triggered by the activation of pattern-recognition receptors (PRRs). The Arabidopsis PRR FLAGELLIN-SENSING 2 (FLS2) senses bacterial flagellin and initiates immune signaling through association with BAK1. The molecular mechanisms underlying the attenuation of FLS2 activation are largely unknown. We report that flagellin induces recruitment of two closely related U-box E3 ubiquitin ligases, PUB12 and PUB13, to FLS2 receptor complex in Arabidopsis. BAK1 phosphorylates PUB12 and PUB13 and is required for FLS2-PUB12/13 association. PUB12 and PUB13 polyubiquitinate FLS2 and promote flagellin-induced FLS2 degradation, and the pub12 and pub13 mutants displayed elevated immune responses to flagellin treatment. Our study has revealed a unique regulatory circuit of direct ubiquitination and turnover of FLS2 by BAK1-mediated phosphorylation and recruitment of specific E3 ligases for attenuation of immune signaling.     

内啡肽的生理功能及其与针灸的关系

本文综述了内啡肽（又称类阿片样肽）作为神经，内分泌、免疫系统的共同信使在动物体内的生理作用，包括参与镇痛过程、调节消化功能、调节生殖内分泌功能以及参与机体免疫过程等几个方面。同时论述了内啡肽与针刺和激光针灸的关系。     

The antibacterial lectin RegIIIgamma promotes the spatial segregation of microbiota and host in the intestine

The mammalian intestine is home to ~100 trillion bacteria that perform important metabolic functions for their hosts. The proximity of vast numbers of bacteria to host intestinal tissues raises the question of how symbiotic host-bacterial relationships are maintained without eliciting potentially harmful immune responses. Here, we show that RegIIIγ, a secreted antibacterial lectin, is essential for maintaining a ~50-micrometer zone that physically separates the microbiota from the small intestinal epithelial surface. Loss of host-bacterial segregation in RegIIIγ(-/-) mice was coupled to increased bacterial colonization of the intestinal epithelial surface and enhanced activation of intestinal adaptive immune responses by the microbiota. Together, our findings reveal that RegIIIγ is a fundamental immune mechanism that promotes host-bacterial mutualism by regulating the spatial relationships between microbiota and host.     

棘皮动物体腔细胞的研究进展

棘皮动物是在脊索动物后分布在海洋中的第二大后口动物。体腔细胞是棘皮动物机体免疫防御的重要组成部分,发挥着重要的免疫防御作用,具有吞噬包裹、氧化杀灭、创伤修复和凝集等多种防御功能。从体腔细胞类型、功能和发生来源3个方面综述了海星、海胆和海参3种主要棘皮动物的体腔细胞研究进展,以期为棘皮动物体腔细胞免疫防御机制研究提供参考。