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肿瘤免疫中红细胞的作用与地位
白细胞免疫系统在肿瘤的发生发展过程中起着非常重要的作用,过去的研究多只涉及此,而红细胞在其中所起的作用一直受到忽视.1981年Siegel[1]提出了红细胞免疫系统(Red-cell immune system)的新概念,开辟了机体免疫系统的新领域.目前对红细胞免疫功能的表现、机理、调节机制与疾病关系等的研究都取得了一定的进展,红细胞具有免疫功能已是不容质疑的事实,大量研究表明红细胞也具有一定的免疫功能.
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近10年脾虚证与免疫系统关系研究进展
脾虚证与免疫功能关系的研究早见于60年代,江苏新医学院中西医结合研究组及虞佩兰等发现部分脾虚患者的白细胞数偏低,经健脾方药治疗后恢复正常.之后70~80年代科研工作者从不同角度对脾虚证与免疫系统的关系进行了深入的研究.本文将近10年来脾虚证与免疫系统关系的研究综述如下.
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中药对老年性痴呆免疫系统改变的干预作用
探寻老年性痴呆(Alzheimer′s disease, AD)发生的确切病理机制及有效防治药物,成为整个医药学界的重要课题。近几年来关于免疫系统改变与老年人身体健康直接相关的证据越来越充分,其作用机理和中草药在调节免疫及细胞因子方面显现出来的独特优势,已为世人所瞩目。以下结合文献报道的研究成果,试分析探讨中药在这方面对AD的可能干预作用。
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高效抗病毒治疗促使艾滋病患者免疫功能重建
The characteristics of AIDS is that HIV infection induces CD4 + T cell defects that includes a quantitave CD4 + T cells depletion and a loss of T helper cells function leading to a progressive immune deficiency. Early report indicated that this immune deficiency was irreversible, even with the antiretroviral therapies. More recently, however, clinical benifits of hightly active antiretroviral therapies (HAART) are increasingly evidenced by resolving opportunistic infections and malignancies, as well as declining hospitalization and mortality rates. This suggests that potent and sustained suppression of viral replication, at least to some extent, is associated with reconstitution of the immune system even in adult patients treated at advanced stages of the disease. Such immune reconstitution which was demonstrated firstly by a French reseach group includes (the group leader is Pr Brigitte Autran)(1) a rapid rise in CD4 + and CD8+ T cells followed by a slower CD4 + T cell increase; (2) a rapid rise in memory CD4 + T cells during the first three months of treatment by late increase in naive T cells coexpressing CD45RA and CD62L molecules after 3 months of efficient antiviral treatment;(3) a significant reduction of CD4 and CD8 activation markers in parallel to plasma virus load reduction;(4) a restoration in CD4 + T cell reactivity to recall antigens. These observations open new perspectives for the understanding of CD4 + T cells deficiency and therapeutic strategies of HIV infection. In the present review we will address some of the questions raised by immune restoration with HAART when administered at advanced stages of the disease.
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HIV感染消化道黏膜的发病机制
近年研究表明,黏膜是执行局部特异性免疫功能的主要场所,称为黏膜免疫系统(mucosal immune system,MIS).MIS分为两大部分:有结构的黏膜滤泡和无结构的弥散淋巴组织.抗原由黏膜滤泡进入MIS,被抗原提呈细胞捕获、处理并提呈给T、B细胞,引起免疫应答.浆细胞和致敏淋巴细胞通过归巢机制迁移至弥散淋巴组织,并在此发挥生物学功能.
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编码基因pac的DNA疫苗经胃肠粘膜免疫SD鼠的研究
变形链球菌(Streptococcus mutans, S.mutans)是主要的致龋菌,细菌表面蛋白PAc是其主要的毒力因子之一.抗PAc抗体能有效阻止S.mutans在牙面的非蔗糖依赖性粘附,从而可以预防龋病的发生.DNA防龋疫苗的成功研制[1,2],给免疫防龋的粘膜免疫提供了崭新的思路.核酸疫苗经粘膜免疫可以通过共同粘膜免疫系统(common mucosal immune system, CMIS)诱导循环及粘膜特异性抗体的反应,更重要的是粘膜IgA的应答,这无疑是免疫防龋的关键所在.本实验用bupivacaine(布比卡因)作为编码变形链球菌表面蛋白pac基因的表达质粒pCIA-P的载体,经由胃、直肠粘膜免疫SD鼠,评价DNA复合体疫苗的免疫效能,探索合适的防龋途径.
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Symposia Report Immunoglobulin G for the Treatment of Chronic Pain:Report of an Expert Workshop
背景:慢性疼痛的治疗效果仍不理想.尽管现在治疗慢性疼痛的药物种类较多,但许多患者对疗效仍不满意或诉药物的副作用太大.越来越多的证据表明,免疫系统参与了伤害性和神经病理性慢性疼痛的病理过程.设计:在英国利物浦的专题会议上,专家们出示了免疫系统参与慢性疼痛的证据.近来的研究表明,静脉(IVIg)或皮下(SCIg)注射免疫调节药物——多价免疫球蛋白(IgG)可缓解外周神经病理性疼痛和其他疼痛性疾病.专题会议讨论了IVIg和SCIg治疗的适应证、效价比及其副作用.结果:IgG可缓解某些伤害性和神经病理性慢性疼痛,如糖尿病、干燥综合征、纤维肌痛症、复杂性区域疼痛综合征、小儿麻痹后遗症和继发于病理性自身抗体的疼痛.结论:IgG对某些慢性疼痛具有一定的治疗前景.IgG是一种相对安全的治疗方法,副作用少而轻,但价格较贵.今后有必要对IgG治疗顽固性疼痛进行随机对照研究和预测性临床试验.
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肝硬化患者创伤后血清微量可溶性补体受体1型表达水平
补体系统是机体重要的防御系统,正常的补体激活在清除凋亡细胞,参与免疫应答和防御病原体入侵中有重要作用[1].补体系统属于天然免疫系统(innate immune system)的一个组成部分,它的激活可产生多种生物学效应,具有免疫调控、黏附、调理促吞噬、清除免疫复合物(immune complexes,IC)和炎症等作用,都是通过补体受体介导的,如补体系统的过度活化,可造成机体组织损伤等疾病,给身体带来严重危害.
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运动与红细胞免疫功能研究进展
运动对机体免疫功能影响的研究已引起国内外广泛关注.但这类研究多集中于运动对白细胞免疫功能和体液免疫功能的影响上,运动与红细胞免疫功能的关系,国内外文献报道较少.以往认为,红细胞只参与呼吸功能.1953年Nelson[1]发现人类红细胞能黏附免疫复合物(immune complex,IC),促进吞噬细胞对其清除.1981年美国生殖免疫学家Siegel提出了"红细胞免疫系统(Red Cell Immune System)"概念[2],随后人们对红细胞免疫的研究取得了突破性进展,研究发现红细胞有许多与免疫有关的物质,数目众多,自成系统.近年来,随着红细胞免疫功能研究的深入,运动与红细胞免疫功能的关系已越来越引起人们的兴趣和重视.
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专题演讲-W3药物和环境毒物的免疫毒性与神经毒性
Toxicity to the immune system encompasses suppression or enhancement of the immune response. Suppression of the immune response can lead to decreased host resistance to infectious agents or tumor cells. Enhancing the immune response can exaggerate autoimmune diseases or hypersensitivity.
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海洛因依赖者神经-内分泌-免疫功能损伤
海洛因,亦称盐酸二乙酰吗啡,其主要成分为二乙酰吗啡,是目前滥用流行广泛、对人体影响严重的阿片类毒品.海洛因依赖者则是因长期滥用海洛因而引起生理、心理综合受创的特殊群体.海洛因吸食带来的短暂欣快感是导致吸食者不断吸毒的重要驱动因素;一旦对毒品形成依赖,骤然停药就会产生无法忍受的戒断症状,因此很难戒除;即使成功消除戒断症状,但"心瘾"未除,也会导致复吸的发生.已证实,戒断症状是产生心瘾而终导致复吸的常见原因,而海洛因依赖者戒断症状又与神经、内分泌、免疫系统均有一定关系[1],因此,研究海洛因依赖者神经、内分泌、免疫系统损伤原因及三大系统间相互影响的关系对复吸的防治有重要意义.
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中药免疫调节及抑瘤作用研究进展
机体的免疫功能异常可导致多种疾病(如感染、恶性肿瘤、变态反应等)的发生.我国古代医学已经具有免疫学的概念,如<内经>中提到的"正气存内,邪不可干"的论点,其中的"正气"即与人体的免疫功能有关,而"邪气"则与现代医学中的病原微生物、自身变性抗原和突变细胞等类似.不但中医学有一套与现代免疫学相符合的理论体系,而且随着对中药药理学的研究,发现许多中药在调节机体的免疫功能、抗感染、抗肿瘤等方面也有其独特的疗效,且其作用与药物种类、成分、配伍及剂量有关.
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病毒性心肌炎的免疫研究进展
病毒性心肌炎(viral myocarditis,VMC)是指病毒感染引起的心肌细胞变性坏死和间质炎性细胞浸润及纤维渗出为主要病理变化的一种常见病.20世纪70年代以来,国内外发病均有增多趋势,在急性病毒感染后大约有5%的人群发病[1],多数情况下为轻中型临床表现.但也可急性暴发所致猝死,部分呈慢性持续感染,遗留顽固性心律失常、慢性心功能不全.近来资料还证实本病与扩张型心肌病的发生密切相关[2].虽然进行了大量的研究,但该病的发病机制至今仍不太清楚,一般认为与病毒直接侵犯心脏和机体的免疫反应损伤有关.本文拟就该病的免疫研究进展综述如下.
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女性生殖道局部黏膜免疫微环境
1 女性生殖道黏膜免疫系统黏膜免疫系统(Mucosal immune system, MIS)是指分布于呼吸道、胃肠道、泌尿生殖道黏膜及一些外分泌腺体的淋巴组织,是执行局部特异性免疫功能的主要场所.黏膜免疫系统在结构和功能上均不同于系统免疫系统,是机体免疫系统的重要组成部分.女性生殖道黏膜因受性激素影响及缺乏典型的集合淋巴结,是一个独特的免疫位点.黏膜表面同时存在固有和适应性免疫保护;固有免疫成分包括黏液层,上皮间紧密连接,抗微生物肽,固有免疫细胞以及各种分泌因子等[1,2].适应性免疫应答主要由T、B淋巴细胞完成.触发的固有免疫可作为桥梁,将适应性免疫联系起来,产生病原体特异的体液/细胞免疫应答.
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红细胞的免疫功能及影响因素
红细胞是血液中含量多的一种有形成分.传统认为,红细胞功能主要有两种:一为运输氧和二氧化碳,即呼吸功能;一为对机体代谢所产生的酸碱物质起缓冲作用,即缓冲功能.随着科学的进步和发展,1981年美国的Siegel在前人研究的基础上提出了"红细胞免疫系统"(Red Cell Immune System,RCIS)的新概念[1],更新了人们对红细胞功能的认识,促进了红细胞免疫研究工作的迅速发展.研究人员发现,红细胞具有很多与免疫有关的物质,如CR1、CR8、LFA-3、DAF、MCP、SOD酶等[2-3],不仅具有识别、粘附、杀伤抗原,清除免疫复合物,参与机体免疫调控的作用,而且其自身存在完整的自我调节控制系统,是机体免疫系统的重要组成部分.本文就红细胞的免疫功能及红细胞免疫功能的影响因素的新研究作一综述.
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肾综合征出血热患者血液透析前后红细胞免疫功能的检测及临床意义
自1981年美国生殖免疫学家Siegel提出"红细胞免疫系统"(The red cell immune system)的新概念后,引起国内外学者的极大关注,开拓了机体免疫系统新领域,许多学者对其表达、机制、调节因子等进行了大量研究[1].但是,在肾综合征出血热(HFRS)患者进行血液透析过程中红细胞免疫功能如何变化却研究较少.因此,对我院HFRS患者血液透析前后的红细胞免疫功能进行了检测和分析,现报告如下.
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前言——重视老年免疫系统疾病的诊治
随着免疫学和老年病学研究进展,老年免疫疾病日益为广大医务工作者所重视.本期重点介绍了与老年免疫系统相关的某些风湿免疫病的诊治特点.
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自体外周血造血干细胞移植治疗重症天疱疮三例
目的 探讨自体外周血造血干细胞移植治疗天疱疮的疗效及安全性.方法 选择经糖皮质激素、免疫抑制剂等治疗6个月以上病情仍难以控制或病情进展、且出现治疗相关并发症的3例寻常型天疱疮患者进行自体外周血造血干细胞移植治疗,并随访5年以上.3例中男1例,女2例,平均年龄27.3(21~39)岁.造血干细胞的动员方案为环磷酰胺4g/m2、重组人粒细胞集落刺激因子(G-CSF)、利妥昔单抗375 mg/m2;预处理方案为环磷酰胺50 mg·kg-1·d-1连用4d(移植前第6天到移植前第3天)、抗胸腺细胞球蛋白2.5 mg·kg-1·d-1连用4d(移植前第3天至移植当天)、利妥昔单抗600 mg/d于移植当天和移植后第7天静脉滴注.结果 3例天疱疮患者均获得成功植入,平均植活时间白细胞13.3 d(11 ~ 16d),血小板16.3 d(16~ 17d).监测各项免疫指标及相关抗体未见异常,免疫重建良好.随访期间,所有患者无严重并发症,生活质量较前明显提高.结论 自体外周血造血干细胞移植可能是治疗天疱疮有效且安全的新方法之一.
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免疫调节T细胞的基础理论及临床应用
Recently,major advances have been made in our understanding of a naturally occurring lymphocyte subset called regulatory T (Treg) cells that are used by the immune system to perform antigen- or tissuespecific immunosuppression[1-6].They play indispensable roles in maintaining health since their deficiency in mice or humans causes fatal inflammatory diseases[1-6].They may also be directly involved in the development of autoimmune diseases since their numbers and/or functions are reduced in patients studied by several groups[7-11].More importantly,a number of laboratories including ours have shown that adoptive transfer of antigen-specific Treg cells effectively prevents,and ameliorates ongoing,experimental models of autoimmune diseases such as multiple sclerosis[12-20].
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Sepsis and septic shock have continued to produce significant morbidity and mortality, in recent times, in acutely injured patients as well as patients in the intensive care units despite advances in antibiotic therapy and in the cardi ovascular and pulmonary support for these patients. This emphasizes the need to gain a better understanding of the fundamental mechanisms of the pathogenesis of sepsis syndrome in the critically ill or injured patients. The present knowled ge of the mechanisms of septic pathogenesis clearly indicates involvement of mod ulations in the functions of the cells of body's immune defense system, namely, monocytes/macrophages, polymorphonuclear leukocytes, and lymphocytes. Most of su ch knowledge has been derived from laboratory experiments in animal models of se ptic injury, or from studies of immune-system cells, in vitro. Clinical stud ies have also supported the role of immune perturbations. Yet, to date, very few the rapeutic approaches are available to effectively counter the sepsis-related immu ne disturbances. Functional modulations in the immune system cells, in the injured/septic hos ts, can exert not only adaptive/beneficial effects but also profoundly adverse effects on the non-immune-system cells such as endothelial, epithelial, neurona l, endocrine, neuro-endocrine, smooth muscle, skeletal muscle, and cardiac muscl e cells. The primary functional modulation in the immune-system cells after inju ry or with critical illness is activation of such cells via molecules from pat hogens, for example, lipopolysaccharide from gram negative organisms, lipoteic hoic acid/peptidoglycan from gram positive organisms, or zymosan from fungi. Suc h pathogenic molecules activate monocytes and tissue macrophages to result in th e expression and release of cytokine mediators (TNFα, IL-1, IL-6, IL-8, and IL- 10), as well as certain lipid mediators (PGE2, LTB4, PAF). While these media tors could play a host-defense role in support of the host via containment/destr uctio n of the pathogens, they could also exert detrimental effects in the host and co ntribute to host morbidity and mortality. Some of these mediators (TNFα, IL-1, IL-6, IL-8, LTB4, PAF) have been shown to be “pro-inflammatory”,and to potenti al ly exert a harmful effect on non-immune cell systems such as endothelial cells, epithelial cells, and muscle cells. Among the pro-inflammatory mediators, TNFα a nd IL-1 could play major harmful roles, and thus contribute to the injured host morbidity and mortality. Mediators, IL-10 and PGE2 have been shown to be “an ti-inflammatory” and to potentially contribute to a dreadful state of immuno-s uppression in the injured hosts, which can also lead to morbidity and mortality. Whi ch is worse, a harmful pro-inflammatory phase or harmful immuno-suppression ? Or Which occurs first, a harmful pro-inflammatory condition or a harmful immuno-su ppression? These are questions which can not be definitively answered for the g eneral population of critically ill/injured patients. It is reasonable to assum e that the answers to these question would vary from one patient subset to anot her patient subset. Thus, whether to treat the patient with a putative anti-pro- inflammatory agent or with a putative anti-anti-inflammatory agent remai ns unresolved for the general sepsis patient population. Paradoxically, TNFα, IL-1, and other pro-inflammatory mediators under certa in circumstances may serve as natural “blockers” of immuno-suppression or “pr omoters” of immune stimulation. This may be true in the case of some of the se ptic patients. Understandably, these patients should not be treated with anti-pro-inf lammatory agents. On the other hand, the anti-inflammatory mediators such as PGE 2, IL-10, and certain other naturally occurring antagonists of TNFα and IL-10 a ctions (TNFα, and IL-1 receptor antagonists) could not only be producing a cert ai n level of immune-suppression but also serving as important feed back controller of the pro-inflammatory mediators. Thus some of the naturally occurring anti-I nflammatory agents could indeed serve as adaptive/beneficial “anti-pro-inflamma tory”, therapeutic agents in certain subset of sepsis patients. Although there is little doubt that effective therapeutic control of the sep sis syndrome could be achieved via appropriate modulation of the cells of the I mmune system, at the present time we do not have an immune therapeutic regimen w hich can singly be efficacious for the general population of patients with the s eptic complication. This implies that before an effective treatment of sepsis p atients, the patients must be identified, by some diagnostic procedure, as to wh ether they need an anti-pro-inflammatory therapy or an anti-anti-inflammatory th erapy. Thus, although immuno-therapy of sepsis remains promising, its efficacy a waits further investigative work particularly through clinical studies in sepsis patients.