4 Cytokines in juvenile chronic arthritis

MB, BS, BSc, PhD, FRCP, FRCPCH Patricia Woo (Professor of Paediatric Rheumatology)
{"title":"4 Cytokines in juvenile chronic arthritis","authors":"MB, BS, BSc, PhD, FRCP, FRCPCH Patricia Woo (Professor of Paediatric Rheumatology)","doi":"10.1016/S0950-3579(98)80016-2","DOIUrl":null,"url":null,"abstract":"<div><p>Cytokines are important mediators of the immune response as well as the inflammatory response. Those concerned primarily with cell growth, differentiation and activation of cells within the immune system are called interleukins, of which there are now 18. Exposure to antigenic and environmental stimuli causes T cells to differentiate and polarise into Th1 or 2-like cells with different cytokine profiles, and requiring different cytokines for differentiation (IL-12 for Th1 and IL-4 for Th2). Homeostasis is usually restored as these cells are mutually inhibitory. Autoimmune diseases have been associated with a persistent imbalance with more Th1-like cells, which are thought to contribute to pathology. With regard to juvenile chronic arthritis (JCA), there is some preliminary evidence of this imbalance in the oligoarticular subgroup. Imbalance of pro-inflammatory cytokines, IL-1 and TNF with their natural inhibitors has also been shown to contribute to persistence of inflammation. In the case of JCA, there has been some evidence that these imbalances could account for some of the disease phenotypes. Furthermore, the tendency to imbalance is genetically determined.</p></div>","PeriodicalId":77032,"journal":{"name":"Bailliere's clinical rheumatology","volume":"12 2","pages":"Pages 219-228"},"PeriodicalIF":0.0000,"publicationDate":"1998-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0950-3579(98)80016-2","citationCount":"14","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bailliere's clinical rheumatology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0950357998800162","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 14

Abstract

Cytokines are important mediators of the immune response as well as the inflammatory response. Those concerned primarily with cell growth, differentiation and activation of cells within the immune system are called interleukins, of which there are now 18. Exposure to antigenic and environmental stimuli causes T cells to differentiate and polarise into Th1 or 2-like cells with different cytokine profiles, and requiring different cytokines for differentiation (IL-12 for Th1 and IL-4 for Th2). Homeostasis is usually restored as these cells are mutually inhibitory. Autoimmune diseases have been associated with a persistent imbalance with more Th1-like cells, which are thought to contribute to pathology. With regard to juvenile chronic arthritis (JCA), there is some preliminary evidence of this imbalance in the oligoarticular subgroup. Imbalance of pro-inflammatory cytokines, IL-1 and TNF with their natural inhibitors has also been shown to contribute to persistence of inflammation. In the case of JCA, there has been some evidence that these imbalances could account for some of the disease phenotypes. Furthermore, the tendency to imbalance is genetically determined.

4细胞因子在青少年慢性关节炎中的作用
细胞因子是免疫反应和炎症反应的重要介质。那些主要与免疫系统内细胞生长、分化和活化有关的物质被称为白细胞介素,目前有18种。暴露于抗原和环境刺激会导致T细胞分化并分化为具有不同细胞因子谱的Th1或2样细胞,并且需要不同的细胞因子来分化(IL-12用于Th1, IL-4用于Th2)。当这些细胞相互抑制时,通常会恢复体内平衡。自身免疫性疾病与th1样细胞的持续不平衡有关,这被认为是导致病理的原因。关于青少年慢性关节炎(JCA),有一些初步证据表明这种不平衡存在于少关节亚群中。促炎细胞因子,IL-1和TNF与其天然抑制剂的不平衡也被证明有助于炎症的持续存在。在JCA的情况下,有一些证据表明这些不平衡可以解释一些疾病表型。此外,失衡的趋势是由基因决定的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信