T cell Repertoire Profiling and the Mechanism by which HLA-B27 Causes Ankylosing Spondylitis.

IF 5.7 2区 医学 Q1 RHEUMATOLOGY Current Rheumatology Reports Pub Date : 2022-12-01 Epub Date: 2022-10-05 DOI:10.1007/s11926-022-01090-6
Jose Garrido-Mesa, Matthew A Brown
{"title":"T cell Repertoire Profiling and the Mechanism by which HLA-B27 Causes Ankylosing Spondylitis.","authors":"Jose Garrido-Mesa,&nbsp;Matthew A Brown","doi":"10.1007/s11926-022-01090-6","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of review: </strong>Ankylosing spondylitis (AS) is strongly associated with the HLA-B27 gene. The canonical function of HLA-B27 is to present antigenic peptides to CD8 lymphocytes, leading to adaptive immune responses. The 'arthritogenic peptide' theory as to the mechanism by which HLA-B27 induces ankylosing spondylitis proposes that HLA-B27 presents peptides derived from exogenous sources such as bacteria to CD8 lymphocytes, which subsequently cross-react with antigens at the site of inflammation of the disease, causing inflammation. This review describes findings of studies in AS involving profiling of T cell expansions and discusses future research opportunities based on these findings.</p><p><strong>Recent findings: </strong>Consistent with this theory, there is an expanding body of data showing that expansion of a restricted pool of CD8 lymphocytes is found in most AS patients yet only in a small proportion of healthy HLA-B27 carriers. These exciting findings strongly support the theory that AS is driven by presentation of antigenic peptides to the adaptive immune system by HLA-B27. They point to new potential approaches to identify the exogenous and endogenous antigens involved and to potential therapies for the disease.</p>","PeriodicalId":10761,"journal":{"name":"Current Rheumatology Reports","volume":null,"pages":null},"PeriodicalIF":5.7000,"publicationDate":"2022-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9666335/pdf/","citationCount":"13","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Rheumatology Reports","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s11926-022-01090-6","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2022/10/5 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"RHEUMATOLOGY","Score":null,"Total":0}
引用次数: 13

Abstract

Purpose of review: Ankylosing spondylitis (AS) is strongly associated with the HLA-B27 gene. The canonical function of HLA-B27 is to present antigenic peptides to CD8 lymphocytes, leading to adaptive immune responses. The 'arthritogenic peptide' theory as to the mechanism by which HLA-B27 induces ankylosing spondylitis proposes that HLA-B27 presents peptides derived from exogenous sources such as bacteria to CD8 lymphocytes, which subsequently cross-react with antigens at the site of inflammation of the disease, causing inflammation. This review describes findings of studies in AS involving profiling of T cell expansions and discusses future research opportunities based on these findings.

Recent findings: Consistent with this theory, there is an expanding body of data showing that expansion of a restricted pool of CD8 lymphocytes is found in most AS patients yet only in a small proportion of healthy HLA-B27 carriers. These exciting findings strongly support the theory that AS is driven by presentation of antigenic peptides to the adaptive immune system by HLA-B27. They point to new potential approaches to identify the exogenous and endogenous antigens involved and to potential therapies for the disease.

Abstract Image

Abstract Image

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
T细胞库谱分析和HLA-B27引起强直性脊柱炎的机制。
综述目的:强直性脊柱炎(AS)与HLA-B27基因密切相关。HLA-B27的典型功能是向CD8淋巴细胞呈递抗原肽,导致适应性免疫反应。关于HLA-B27诱导强直性脊柱炎的机制,“关节炎原肽”理论提出,HLA-B27将来自细菌等外源性来源的肽呈递给CD8淋巴细胞,这些肽随后与疾病炎症部位的抗原交叉反应,引起炎症。本文综述了AS中涉及T细胞扩增谱的研究结果,并讨论了基于这些发现的未来研究机会。最近的发现:与这一理论相一致的是,越来越多的数据表明,在大多数AS患者中发现了有限的CD8淋巴细胞池的扩增,但仅在一小部分健康的HLA-B27携带者中发现。这些令人兴奋的发现有力地支持了AS是由HLA-B27向适应性免疫系统呈递抗原肽驱动的理论。他们指出了新的潜在方法来识别外源性和内源性抗原,并为疾病提供了潜在的治疗方法。
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 去求助
来源期刊
CiteScore
11.20
自引率
0.00%
发文量
41
期刊介绍: This journal aims to review the most important, recently published research in the field of rheumatology. By providing clear, insightful, balanced contributions by international experts, the journal intends to serve all those involved in the care and prevention of rheumatologic conditions. We accomplish this aim by appointing international authorities to serve as Section Editors in key subject areas such as the many forms of arthritis, osteoporosis and metabolic bone disease, and systemic lupus erythematosus. Section Editors, in turn, select topics for which leading experts contribute comprehensive review articles that emphasize new developments and recently published papers of major importance, highlighted by annotated reference lists. An international Editorial Board reviews the annual table of contents, suggests articles of special interest to their country/region, and ensures that topics are current and include emerging research. Commentaries from well-known figures in the field are also occasionally provided.
期刊最新文献
How to Distinguish Non-Inflammatory from Inflammatory Pain in RA? Telemedicine for the Care of Patients with Idiopathic Inflammatory Myopathies: Experience, Insights and Future Directions from the International Myositis Assessment and Clinical Studies Telemedicine Scientific Interest Group. Treatment of Reactive Arthritis with Biological Agents. Recent Updates on the Pathogenesis of Inflammatory Myopathies. Rheumatoid Arthritis-Associated Interstitial Lung Disease (RA-ILD): Update on Prevalence, Risk Factors, Pathogenesis, and Therapy.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1