呼吸道菌群与黏膜免疫在哮喘发病机制中的作用

支气管哮喘(简称哮喘)是儿童常见的慢性呼吸道疾病。随着高通量测序技术的发展,人们发现哮喘的发生、发展与人体微生物群的失衡密切相关。研究表明呼吸道菌群的变化可对宿主黏膜免疫系统产生显著影响。呼吸道菌群可通过特定的作用机制参与哮喘气道炎症、气道高反应性和气道重塑等病理生理过程。该文就呼吸道菌群与黏膜免疫在哮喘发病机制中发挥...     

儿童呼吸道过敏性疾病与感染

近年来,随着人类生活环境的变化,呼吸道过敏性疾病,如过敏性鼻炎、婴幼儿喘息、过敏性哮喘等的发病率不断上升,影响儿童的生活质量,为家庭、社会带来沉重的负担。微生物感染,如病毒、细菌、支原体/衣原体、真菌、寄生虫等感染,均能通过免疫机制来调节呼吸道过敏性疾病的发生、发展。为加强理解呼吸道过敏与微生物感染之间的关系及其相关机...     

肠黏膜先天性免疫的研究进展

肠道是人体免疫系统的重要组成部分，在接触大量的食物和消除病原微生物的过程中，肠黏膜屏障起了重大的作用。由生理性屏障结构和天然存在的抗微生物分子构成的先天性免疫，是宿主肠道防御系统的重要组成部分。     

肠黏膜先天性免疫的研究进展

肠道是人体免疫系统的重要组成部分,在接触大量的食物和消除病原微生物的过程中,肠黏膜屏障起了重大的作用。由生理性屏障结构和天然存在的抗微生物分子构成的先天性免疫,是宿主肠道防御系统的重要组成部分。     

儿童反复呼吸道感染的支气管黏膜免疫和气道高反应性变化

反复呼吸道感染(recurrent respiration tract infection,RRTI)是儿童常见的呼吸道疾病,常见的原因有免疫功能低下、先天畸形、营养物质缺乏、慢性疾病以及感染疾病治疗不彻底等。RRTI与呼吸道黏膜免疫改变、气道高反应性及过敏有关。     

黏膜免疫异常与小儿慢性腹泻

小儿慢性腹泻是目前临床上一个很棘手的问题。其病因非常复杂，各种感染、营养物质过敏、酶缺陷、免疫缺陷、药物因素、先天畸形等均可引起迁延不愈的腹泻。其发病机制中两个重要原因为：1，原发性肠上皮细胞异常；2、免疫异常。导致小儿慢性腹泻病的免疫异常亦包括：1、不能抵御病原微生物侵袭；2．对原本应耐受食物中的各种抗原产生免疫反应。     

支气管哮喘发病的黏膜免疫机制研究进展

无论哮喘发作期还是缓解期,黏膜免疫系统均会对其作出相应的应答反应。γδT细胞所分泌细胞因子在种类上和数量上均会有所变化,肥大细胞脱颗粒亦会受到影响,IgA、肺表面活性蛋白、防御素等活性物质也异于正常。因此,哮喘发病黏膜免疫机制是复杂的和多环节的。     

Th17细胞在肠黏膜免疫中的作用

肠黏膜是人体最大的淋巴器官,它与呼吸道黏膜、泌尿生殖道黏膜等一起构成机体的第一道防御体系.肠黏膜经常抵御细菌、病毒、食物抗原、非甾体类抗炎药等的侵袭,若肠黏膜免疫系统遭受破坏,机体发生感染性疾病、自身免疫性疾病等.因此,肠黏膜免疫功能正常对机体的健康非常重要.Th17细胞是近年来发现的一类不同于Th1和Th2细胞的T细...     

短链脂肪酸与食物过敏的肠道黏膜免疫

食物过敏的发病机制、诊断标准以及治疗方案仍需进一步探究.短链脂肪酸是肠道菌群的代谢产物之一,关于其免疫调节作用的研究逐渐增多并且已经应用于某些免疫相关疾病的临床治疗.为全面了解短链脂肪酸对食物过敏的肠道黏膜免疫调节以及潜在的治疗作用,文章综述了食物过敏的肠道黏膜免疫机制、短链脂肪酸与食物过敏的联系,以及短链脂肪酸在其中...     

肠黏膜屏障与粪sIgA及其在相关疾病中的研究进展

肠黏膜屏障能防止肠腔内有害物质穿过肠黏膜进入体内其他组织器官和血液循环,而粪便中sIgA是肠黏膜屏障中重要部分,是肠黏膜免疫屏障的主要免疫球蛋白,是维持肠道黏膜稳态的第一道防线,具有强化肠道的免疫屏障、阻止肠道病原体入侵、减轻肠道炎症反应等生物学功能.该文对粪便sIgA在相关疾病的研究进行综述,通过测定粪便中sIgA含量为相关疾病诊断及治疗提供理论依据.     

Mucosal immunity and strategies for novel microbial vaccines

Infectious diseases continue to be the leading cause of morbidity and mortality worldwide. Increased awareness of the fact that mucosal membranes are the most frequent portals of entry of pathogenic microorganisms has prompted studies aimed at the development of vaccination protocols and antigen delivery systems that would lead to an increased protection of mucosae. Although systemic and strictly local immunizations are of limited effectiveness in the induction of mucosal protection, ingestion or inhalation of antigens results in a generalized immune response manifested by the appearance of specific antibodies of the secretory immunoglobulin (Ig) isotype in external secretions due to the dissemination of IgA precursor cells from IgA-inductive lymphoid tissues. Furthermore, additional inductive sites strategically positioned at the opening of the respiratory and digestive tracts may also be suitable targets for induction of immune responses at desired effector sites. To prevent degradation and the increase of ingested antigens absorption, novel strategies including enclosure of antigens into biodegradable microspheres, liposomes or their expression in viral and bacterial vectors and plants are currently being considered. Forthcoming technological advances in antigen preparation and routes of delivery will undoubtedly have a profound impact on immunization practices in the future.     

Mucosal Neuromas and Plexiform Neurofibromas: An Immunocytochemical Study

Mucosal neuromas (MN), a component of multiple endocrine neoplasia (MEN) type IIb, may be confused histologically with plexiform neurofibromas (PN), a component of neurofibromatosis. The ability to distinguish between these two markers for different genetic diseases is crucial, as the risk of development of medullary thyroid carcinoma and pheochromocytoma in affected patients with MEN IIb is great. We studied two cases each of MN and PN by immunocytochemistry (IC). Epithelial membrane antigen (EMA) proved to be the most useful marker. MN consisted of bundles of disorganized and tortuous nerve fibers surrounded by a thickened perineurium that expressed the cellular phenotype EMA(+), S-100(-). PN consisted of enlarged neroe fascicles with a loose myxoid stroma and was EMA negative. Thus, IC highlighted the differing pattern of growth and histogenesis of the proliferating cells in the two lesions and is likely to be especially useful in those lesions with atypical histology.     

Ⅱ型固有淋巴细胞与过敏性疾病研究进展

固有淋巴细胞(innate lymphoid cell,ILC)是人们近些年发现的一类谱系阴性、但可以接受刺激产生炎症因子的免疫细胞.根据其不同的功能将其分为ILC1、ILC2、ILC3三类,其中Ⅱ型固有淋巴细胞(ILC2)因其对寄生虫、哮喘等过敏性疾病具有相关影响而备受关注.该文就ILC2的表型与过敏性疾病的关系进行阐述.     

Mucosal immune response development: breastfeeding and environmental influence

A review of the current knowledge of mucosal immune response development indicates that migration of immunocytes to mucosal surfaces is an early event during fetal life. The morphologic development of gut-associated lymphoid tissues (lymphoid follicles, Peyer's patches and tonsils) occurs from 11-20 weeks' gestation upwards. But they are active only after birth, when usually antigenic challenge takes place. The complete development of secretory immunity is a postnatal achievement. In infancy, some environmental factors such as feeding and oral antigenic challenge seems to modulate immune response development. Breastfeeding, by means of antiinfectious, antiinflammatory and immunomodulating properties, besides completing infant secretory immunity, also stimulates immunological maturation on mucosal surfaces.     

调节性B细胞与变态反应性疾病

近年来,对于免疫机制的研究越来越关注于负向调节方面.早些年更多关注于调节性T细胞,但最近也发现B细胞有亚群对免疫系统起负向调节作用,称之为调节性B细胞.变态反应性疾病存在机体的过度免疫且多迁延不愈,其重要的原因就是个体的负向调节机制发生变化.调节性B细胞作为一种重要的调节性细胞,可能在变态反应性疾病的发生和发展中起重要的抑制作用,并且在变态反应性疾病的治疗中可能存在广阔前景.     

剖宫产与儿童过敏性疾病

文章介绍了新生儿肠道菌群的形成过程,肠道菌群的构成及其对人体免疫系统的调控作用;剖宫产和非母乳喂养方式对新生儿肠道菌群的不良影响,由此而发生过敏症等疾病的机制.简要介绍了益生菌的定义,其生理学意义和治疗及预防婴儿过敏性疾病的作用.     

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1原发性免疫缺陷病的快速诊断和免疫重建治疗原发性免疫缺陷病(PID)的诊治越来越受到儿科医师重视,我国(未包括台、澳地区)已确诊PID逾200例。建立网络登记系统及时发现新的可疑病例并早期诊断十分重要。中华儿科学会免疫学组委托香港大学儿童与青少年医学系免疫学家筹建了PID登记随访网站(http:/paed.hku.hk/study3/pid),以便全国儿科医师呈递可疑PID病例的临床资料,并在互联网上进行讨论、会诊。PID的诊治更需要社会各界的重视和参与,免疫学组与热心于公益事业的企业合作建立了中国PID关爱中心公益网站(www.pid.rons-en.com),旨在…     

EB病毒感染及其免疫反应

EB病毒感染范围广,且具有强大的增长转化能力,能够转化为若干恶性疾病.该病毒的感染大多为隐性感染,没有明显的临床症状.目前越来越多的研究发现,细胞免疫,尤其是T细胞应答在控制感染中发挥着重要的作用.     

IgE response and its regulation in allergic diseases

The distinguishing feature of the allergic person is his or her elevation of serum IgE. This propensity to develop a sustained IgE response is determined genetically. The biologic effects of IgE are mediated via Fc receptors (Fc epsilon R) present on mast cells and basophils (Fc epsilon R type 1) and subpopulations of monocytes, macrophages, eosinophils, and platelets (Fc epsilon R type 2). Interaction of allergen with IgE on these cells results in receptor "bridging" and the release of histamine and other inflammatory mediators. Fc epsilon R type 2 on lymphocytes and monocytes are upregulated in atopic disease and may play a role in the allergic inflammatory reaction. The activation of B cells to synthesize IgE requires several stages (see Fig. 2). T cells play an important role in the regulation of IgE synthesis. In vitro activation of resting B cells to synthesize IgE requires direct cellular interaction with T cells or the presence of IL4 for activation. The latter effect is inhibited by alpha-interferon. Preactivated B cells are influenced in an isotype-specific manner by T-cell-derived IgE binding factors (IgE-BF), which may act as IgE-potentiating or IgE-suppressive factors, depending on their degree of glycosylation. The regulation of IgE synthesis is an important area of investigation. It provides us with an understanding of the basis of the human allergic response and ultimately may provide the basis for novel strategies in the treatment of allergic diseases.