Formation and clinical effects of anti-drug antibodies against biologics in psoriasis treatment: An analysis of current evidence

IF 9.2 1区 医学 Q1 IMMUNOLOGY Autoimmunity reviews Pub Date : 2024-03-17 DOI:10.1016/j.autrev.2024.103530
Xiaoying Sun , Ziyang Cui , Qingyun Wang , Liu Liu , Xiaojie Ding , Jiao Wang , Xiaoce Cai , Bin Li , Xin Li
{"title":"Formation and clinical effects of anti-drug antibodies against biologics in psoriasis treatment: An analysis of current evidence","authors":"Xiaoying Sun ,&nbsp;Ziyang Cui ,&nbsp;Qingyun Wang ,&nbsp;Liu Liu ,&nbsp;Xiaojie Ding ,&nbsp;Jiao Wang ,&nbsp;Xiaoce Cai ,&nbsp;Bin Li ,&nbsp;Xin Li","doi":"10.1016/j.autrev.2024.103530","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Formation of anti-drug antibodies (ADAs) against biologics is an important cause of psoriasis treatment failure.</p></div><div><h3>Objective</h3><p>This study aimed to summarize the characteristics of ADAs formation under different biological therapies and the influence of ADAs on the clinical effects and safety of biologics in patients with psoriasis.</p></div><div><h3>Methods</h3><p>PubMed, Embase, and Web of Science databases were searched from their inception to August 2022. Studies on biologics that assessed ADA levels in patients with psoriasis were included. The Cochrane risk-of-bias tool was used to assess the quality of randomized controlled trials (RCTs), the Newcastle-Ottawa Quality Assessment Scale (NOS) for case-control and cohort studies, and the Joanna Briggs Institute (JBI) critical appraisal checklist for single-arm studies. We calculated the pooled incidence with a random-effects model using R software. Subgroup analyses revealed that differences in patient characteristics, disease conditions, study design, and immunoassays may influence ADA generation and detection.</p></div><div><h3>Results</h3><p>The analysis included 86 studies, with a total population of 42,280 individuals. The pooled ADA rates were 0.49%, 2.20%, 2.38%, 4.08%, 7.38%, 7.94%, 14.29%, 21.93%, 29.70%, 31.76%, and 39.58% for secukinumab, etanercept, brodalumab, ustekinumab, tildrakizumab, guselkumab, ixekizumab, risankizumab, infliximab, adalimumab, and bimekizumab, respectively. &gt;70% (95% CI, 0.71–0.81) of ADAs against adalimumab were neutralizing antibodies, and over 70% of ADAs against secukinumab and brodalumab were transient. Concomitant methotrexate therapy with tumor necrosis factor-α (TNF-α) inhibitors decreased ADA levels. Lower infliximab doses and intermittent therapy with interleukin (IL)-23 p19 inhibitors increased ADA formation. Additionally, ADA formation under treatment using TNF-α inhibitors and IL-12/23 p40 inhibitors was associated with lower response rates or serum drug levels, but only high ADA titers reduced the clinical effects of IL-17 inhibitors. The occurrence of IL-23 p19 and TNF-α inhibitors has been linked to injection-site reactions.</p></div><div><h3>Conclusions</h3><p>Among the 11 biologics, secukinumab, etanercept, and brodalumab resulted in the lowest ADA formation rates. Immunogenicity contributes to lower biological efficacy and a higher likelihood of injection-site reactions. Low doses, intermittent treatment may increase ADA formation. An appropriate biologic should be selected based on the ADA formation rate and course of treatment.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 4","pages":"Article 103530"},"PeriodicalIF":9.2000,"publicationDate":"2024-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autoimmunity reviews","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1568997224000211","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background

Formation of anti-drug antibodies (ADAs) against biologics is an important cause of psoriasis treatment failure.

Objective

This study aimed to summarize the characteristics of ADAs formation under different biological therapies and the influence of ADAs on the clinical effects and safety of biologics in patients with psoriasis.

Methods

PubMed, Embase, and Web of Science databases were searched from their inception to August 2022. Studies on biologics that assessed ADA levels in patients with psoriasis were included. The Cochrane risk-of-bias tool was used to assess the quality of randomized controlled trials (RCTs), the Newcastle-Ottawa Quality Assessment Scale (NOS) for case-control and cohort studies, and the Joanna Briggs Institute (JBI) critical appraisal checklist for single-arm studies. We calculated the pooled incidence with a random-effects model using R software. Subgroup analyses revealed that differences in patient characteristics, disease conditions, study design, and immunoassays may influence ADA generation and detection.

Results

The analysis included 86 studies, with a total population of 42,280 individuals. The pooled ADA rates were 0.49%, 2.20%, 2.38%, 4.08%, 7.38%, 7.94%, 14.29%, 21.93%, 29.70%, 31.76%, and 39.58% for secukinumab, etanercept, brodalumab, ustekinumab, tildrakizumab, guselkumab, ixekizumab, risankizumab, infliximab, adalimumab, and bimekizumab, respectively. >70% (95% CI, 0.71–0.81) of ADAs against adalimumab were neutralizing antibodies, and over 70% of ADAs against secukinumab and brodalumab were transient. Concomitant methotrexate therapy with tumor necrosis factor-α (TNF-α) inhibitors decreased ADA levels. Lower infliximab doses and intermittent therapy with interleukin (IL)-23 p19 inhibitors increased ADA formation. Additionally, ADA formation under treatment using TNF-α inhibitors and IL-12/23 p40 inhibitors was associated with lower response rates or serum drug levels, but only high ADA titers reduced the clinical effects of IL-17 inhibitors. The occurrence of IL-23 p19 and TNF-α inhibitors has been linked to injection-site reactions.

Conclusions

Among the 11 biologics, secukinumab, etanercept, and brodalumab resulted in the lowest ADA formation rates. Immunogenicity contributes to lower biological efficacy and a higher likelihood of injection-site reactions. Low doses, intermittent treatment may increase ADA formation. An appropriate biologic should be selected based on the ADA formation rate and course of treatment.

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
银屑病治疗中针对生物制剂的抗药性抗体的形成和临床效果:现有证据分析。
背景:针对生物制剂的抗药性抗体(ADA)的形成是牛皮癣治疗失败的重要原因:针对生物制剂的抗药抗体(ADA)的形成是银屑病治疗失败的重要原因:本研究旨在总结不同生物疗法下ADA形成的特点,以及ADA对银屑病患者使用生物制剂的临床效果和安全性的影响:方法:对 PubMed、Embase 和 Web of Science 数据库从开始到 2022 年 8 月的内容进行了检索。纳入了评估银屑病患者体内 ADA 水平的生物制剂研究。科克伦偏倚风险工具用于评估随机对照试验(RCT)的质量,纽卡斯尔-渥太华质量评估量表(NOS)用于病例对照和队列研究,乔安娜-布里格斯研究所(JBI)关键评估清单用于单臂研究。我们使用 R 软件的随机效应模型计算了汇总发病率。亚组分析表明,患者特征、疾病状况、研究设计和免疫测定方法的不同可能会影响ADA的产生和检测:分析包括 86 项研究,总人数为 42,280 人。secukinumab、etanercept、brodalumab、ustekinumab、tildrakizumab、guselkumab、ixekizumab、risankizumab、infliximab、adalimumab和bimekizumab的合并ADA率分别为0.49%、2.20%、2.38%、4.08%、7.38%、7.94%、14.29%、21.93%、29.70%、31.76%和39.58%。针对阿达木单抗的ADA中>70%(95% CI,0.71-0.81)为中和抗体,针对secukinumab和brodalumab的ADA中超过70%为一过性抗体。甲氨蝶呤与肿瘤坏死因子-α(TNF-α)抑制剂同时治疗会降低ADA水平。较低的英夫利西单抗剂量和白细胞介素(IL)-23 p19抑制剂的间歇治疗会增加ADA的形成。此外,在使用TNF-α抑制剂和IL-12/23 p40抑制剂治疗时,ADA的形成与较低的应答率或血清药物水平有关,但只有高ADA滴度才会降低IL-17抑制剂的临床效果。IL-23 p19和TNF-α抑制剂的发生与注射部位反应有关:在11种生物制剂中,secukinumab、etanercept和brodalumab的ADA形成率最低。免疫原性会降低生物疗效,增加注射部位反应的可能性。小剂量、间歇性治疗可能会增加 ADA 的形成。应根据 ADA 形成率和疗程选择合适的生物制剂。
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
Autoimmunity reviews
Autoimmunity reviews 医学-免疫学
CiteScore
24.70
自引率
4.40%
发文量
164
审稿时长
21 days
期刊介绍: Autoimmunity Reviews is a publication that features up-to-date, structured reviews on various topics in the field of autoimmunity. These reviews are written by renowned experts and include demonstrative illustrations and tables. Each article will have a clear "take-home" message for readers. The selection of articles is primarily done by the Editors-in-Chief, based on recommendations from the international Editorial Board. The topics covered in the articles span all areas of autoimmunology, aiming to bridge the gap between basic and clinical sciences. In terms of content, the contributions in basic sciences delve into the pathophysiology and mechanisms of autoimmune disorders, as well as genomics and proteomics. On the other hand, clinical contributions focus on diseases related to autoimmunity, novel therapies, and clinical associations. Autoimmunity Reviews is internationally recognized, and its articles are indexed and abstracted in prestigious databases such as PubMed/Medline, Science Citation Index Expanded, Biosciences Information Services, and Chemical Abstracts.
期刊最新文献
Anti-lipoprotein lipase antibodies: A review. MOGAD: A comprehensive review of clinicoradiological features, therapy and outcomes in 4699 patients globally. Advancing understanding of autoimmune disease-related interstitial lung disease (AD-ILD): A global perspective on research focus and future directions. Is it time for treat-to-target in antiphospholipid syndrome? Artificial intelligence meets the world experts; updates and novel therapies in autoimmunity - The 14th international congress on autoimmunity 2024 (AUTO14), Ljubljana.
×
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