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Best Practice & Research in Clinical Rheumatology最新文献

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38.3 Primary Immunodeficiencies: When is it not just “JIA” 38.3 原发性免疫缺陷：何时不仅仅是 "JIA"。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.101960
{"title":"38.3 Primary Immunodeficiencies: When is it not just “JIA”","authors":"","doi":"10.1016/j.berh.2024.101960","DOIUrl":"10.1016/j.berh.2024.101960","url":null,"abstract":"<div><div><span>Juvenile Idiopathic Arthritis<span> (JIA) is sometimes considered a diagnosis of exclusion as the name signifies that no cause is evident for this form of arthritis. Despite this JIA has some classical clinical features and many categories are defined based on the phenotype</span></span><strong>.</strong><span> Since there is no diagnostic test for JIA, diseases that can mimic JIA, including Primary Immunodeficiencies (PID) can sometimes be misdiagnosed as JIA. The clues to suspecting PIDs are early age of onset, presence of family history, increased susceptibility to infections, unusual features like urticaria<span>, interstitial lung disease, sensorineural hearing loss and poor response to conventional therapy, amongst others. This review will highlight the basics of PIDs and will discuss PIDs that can present with arthritis and hence can be confused with JIA.</span></span></div></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 101960"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Challenges and complications in juvenile localized scleroderma: A practical approach 幼年局部硬皮病的挑战与并发症：实用方法。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.101987
Clare E. Pain , Kathryn S. Torok
{"title":"Challenges and complications in juvenile localized scleroderma: A practical approach","authors":"Clare E. Pain ,&nbsp;Kathryn S. Torok","doi":"10.1016/j.berh.2024.101987","DOIUrl":"10.1016/j.berh.2024.101987","url":null,"abstract":"<div><div>Juvenile localized scleroderma is characterised by inflammation which drives fibrosis in skin and soft tissues. The more severe subtypes of localized scleroderma such as linear and craniofacial are more common in children. Additionally, extracutaneous involvement is seen in half of all children and is associated with poorer treatment outcomes and health-related quality of life. Evidence for the management of craniofacial and extracutaneous involvement is lacking and therefore poses a challenge to clinicians. This review aims to provide a practical approach to management of these most challenging features of juvenile localized scleroderma through case studies where we present the available evidence, current recommendations and considerations for management.</div></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 101987"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Preface: Pediatric rheumatology 前言：小儿风湿病学。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-09-01 DOI: 10.1016/j.berh.2024.102004
Christiaan Scott, Petra Hissink Muller
{"title":"Preface: Pediatric rheumatology","authors":"Christiaan Scott,&nbsp;Petra Hissink Muller","doi":"10.1016/j.berh.2024.102004","DOIUrl":"10.1016/j.berh.2024.102004","url":null,"abstract":"","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 3","pages":"Article 102004"},"PeriodicalIF":4.5,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142300237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Non-coding DNA variants for risk in lupus 红斑狼疮风险的非编码 DNA 变异。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101937
{"title":"Non-coding DNA variants for risk in lupus","authors":"","doi":"10.1016/j.berh.2024.101937","DOIUrl":"10.1016/j.berh.2024.101937","url":null,"abstract":"<div><p>Systemic Lupus Erythematosus (SLE) is a multifactorial autoimmune disease that arises from a dynamic interplay between genetics and environmental triggers. The advent of sophisticated genomics technology has catalyzed a shift in our understanding of disease etiology, spotlighting the pivotal role of non-coding DNA variants in SLE pathogenesis. In this review, we present a comprehensive examination of the non-coding variants associated with SLE, shedding light on their role in influencing disease risk and progression. We discuss the latest methodological advancements that have been instrumental in the identification and functional characterization of these genomic elements, with a special focus on the transformative power of CRISPR-based gene-editing technologies. Additionally, the review probes into the therapeutic opportunities that arise from modulating non-coding regions associated with SLE. Through an exploration of the complex network of non-coding DNA, this review aspires to decode the genetic puzzle of SLE and set the stage for groundbreaking gene-based therapeutic interventions and the advancement of precision medicine strategies tailored to SLE management.</p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101937"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140013651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Immune checkpoints in autoimmune vasculitis 自身免疫性血管炎中的免疫检查点
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101943
{"title":"Immune checkpoints in autoimmune vasculitis","authors":"","doi":"10.1016/j.berh.2024.101943","DOIUrl":"10.1016/j.berh.2024.101943","url":null,"abstract":"<div><p><span>Giant cell arteritis<span><span><span> (GCA) is a prototypic autoimmune disease with a highly selective tissue tropism for medium and large arteries. Extravascular GCA manifests with intense systemic inflammation and </span>polymyalgia rheumatica; vascular GCA results in vessel wall damage and stenosis, causing </span>tissue ischemia<span>. Typical granulomatous infiltrates in affected arteries are composed of CD4</span></span></span><sup>+</sup><span> T cells and hyperactivated macrophages, signifying the involvement of the innate and adaptive immune system. Lesional CD4</span><sup>+</sup> T cells undergo antigen-dependent clonal expansion, but antigen-nonspecific pathways ultimately control the intensity and duration of pathogenic immunity. Patient-derived CD4<sup>+</sup><span> T cells receive strong co-stimulatory signals through the NOTCH1 receptor and the CD28/CD80-CD86 pathway. In parallel, co-inhibitory signals, designed to dampen overshooting T cell immunity, are defective, leaving CD4</span><sup>+</sup><span> T cells unopposed and capable of supporting long-lasting and inappropriate immune responses. Based on recent data, two inhibitory checkpoints are defective in GCA: the Programmed death-1 (PD-1)/Programmed cell death ligand 1 (PD-L1) checkpoint and the CD96/CD155 checkpoint, giving rise to the “lost inhibition concept”. Subcellular and molecular analysis has demonstrated trapping of the checkpoint ligands in the endoplasmic reticulum, creating PD-L1</span><sup>low</sup><span> CD155</span><sup>low</sup> antigen-presenting cells. Uninhibited CD4<sup>+</sup><span> T cells expand, release copious amounts of the cytokine Interleukin (IL)-9, and differentiate into long-lived effector memory cells. These data place GCA and cancer on opposite ends of the co-inhibition spectrum, with cancer patients developing immune paralysis due to excessive inhibitory checkpoints and GCA patients developing autoimmunity due to nonfunctional inhibitory checkpoints.</span></p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101943"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140871112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dendritic cells and antigen-specific immunotherapy in autoimmune rheumatic diseases 树突状细胞和自身免疫性风湿病中的抗原特异性免疫疗法。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101940
{"title":"Dendritic cells and antigen-specific immunotherapy in autoimmune rheumatic diseases","authors":"","doi":"10.1016/j.berh.2024.101940","DOIUrl":"10.1016/j.berh.2024.101940","url":null,"abstract":"<div><p>Dendritic cells (DCs) are professional antigen-presenting cells and trigger downstream immune responses to antigen while integrating cellular pathogen and damage-associated molecular pattern (PAMP and DAMP) or immunomodulatory signals. In healthy individuals, resting and tolerogenic DCs draining skin and intestine facilitate expansion of regulatory T cells (Treg) to maintain peripheral antigen-specific immune tolerance. In patients with rheumatic diseases, however, DCs activated by PAMPs and DAMPs expand self-reactive effector T cells, including follicular helper T cells that promote the expansion of activated autoreactive B cells, chronic inflammation and end-organ damage. With the development of cellular and nanoparticle (NP)-based self-antigen-specific immunotherapies we here consider the new opportunities and the challenges for restoring immunoregulation in the treatment and prevention of autoimmune inflammatory rheumatic conditions through DCs.</p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101940"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1521694224000111/pdfft?md5=bf169639c49fdd2ca495145dff4e0c7d&pid=1-s2.0-S1521694224000111-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140133185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Potential therapeutic targets of fibrosis in inflammatory rheumatic diseases 炎症性风湿病纤维化的潜在治疗目标。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101945
{"title":"Potential therapeutic targets of fibrosis in inflammatory rheumatic diseases","authors":"","doi":"10.1016/j.berh.2024.101945","DOIUrl":"10.1016/j.berh.2024.101945","url":null,"abstract":"<div><p><span>Fibrosis<span> is commonly associated with chronic rheumatic diseases, and causes substantial morbidity and mortality. Treatment of fibrosis is extremely challenging but is badly needed, as approved antifibrotic therapies fibrosis do not halt its progression, which will be discussed with a focus on </span></span>pulmonary fibrosis<span>. Findings from recent studies indicate several therapeutic targets for treating fibrosis. Interleukin-11 is emerging as a fibrogenic<span> cytokine whose activity can be blocked with neutralizing monoclonal antibodies. Fibroblast activation protein (FAP) is highly expressed by activated fibroblasts in inflammatory and fibrotic tissues. Targeting FAP with different modalities has been extensively explored as adjunct treatment for cancer, which can also apply to treating fibrosis in rheumatic diseases.</span></span></p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101945"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140867478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Granzyme K+ CD8 T cells in autoimmunity 自身免疫中的颗粒酶 K+ CD8 T 细胞
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101930
{"title":"Granzyme K+ CD8 T cells in autoimmunity","authors":"","doi":"10.1016/j.berh.2024.101930","DOIUrl":"10.1016/j.berh.2024.101930","url":null,"abstract":"<div><p>CD8 T cells expressing granzyme K are enriched in synovial tissue from patients with rheumatoid arthritis and in tissues affected by several other autoimmune diseases. The roles these cells play in autoimmune disease is under active investigation, and several recent studies have begun to shed light on this question. Putting this cell type into functional perspective is especially important given their enrichment at the sites of disease. This review summarizes available evidence for the presence of CD8 T cells and other granzyme K-expressing cells in tissues in autoimmune diseases and discusses the effects these cells may have on the pathogenesis of autoimmune conditions.</p></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101930"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139658949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CARD9 in the pathogenesis of axial spondyloarthritis 轴性脊柱关节炎发病机制中的 CARD9。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101964
{"title":"CARD9 in the pathogenesis of axial spondyloarthritis","authors":"","doi":"10.1016/j.berh.2024.101964","DOIUrl":"10.1016/j.berh.2024.101964","url":null,"abstract":"<div><p>Axial spondyloarthritis<span><span><span> (axSpA) has been long classified as an autoimmune disease caused by a breakdown in the ability of the immune system to delineate self from foreign, resulting in self-reactive </span>T cells. The strong </span>genetic<span><span> association of HLA-B27 supports this role for T cells<span>. More recently, genetic and clinical studies indicate a prominent role of the environment in triggering axSpA, including an important role for microbes and the innate immune response. As an example, mutations in genes associated with innate immunity, including the anti-fungal signaling molecule </span></span>Caspase recruitment domain-containing protein 9 (CARD9), have been linked to axSpA susceptibility. Thus, current thought classifies axSpA as a “mixed pattern condition” caused by both autoimmune and autoinflammatory mechanisms.</span></span></p><p>The goal of this review is to convey:</p><ul><li><span>•</span><span><p>Genetic/environmental mediating factors in axSpA</p></span></li><li><span>•</span><span><p>Known roles for CARD9 in anti-fungal immunity versus sterile inflammation</p></span></li><li><span>•</span><span><p>Previously characterized neutrophil-intrinsic roles for CARD9</p></span></li><li><span>•</span><span><p>Studies supporting a role for CARD9<sup>S12N</sup> mutation in promoting axSpA</p></span></li></ul></div>","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101964"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141428220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Immunopathology of inflammatory rheumatic diseases 炎症性风湿病的免疫病理学。
IF 4.5 2区 医学
Best Practice & Research in Clinical Rheumatology Pub Date : 2024-05-01 DOI: 10.1016/j.berh.2024.101980
Xiaofei Shi, Cong-Qiu Chu
{"title":"Immunopathology of inflammatory rheumatic diseases","authors":"Xiaofei Shi,&nbsp;Cong-Qiu Chu","doi":"10.1016/j.berh.2024.101980","DOIUrl":"10.1016/j.berh.2024.101980","url":null,"abstract":"","PeriodicalId":50983,"journal":{"name":"Best Practice & Research in Clinical Rheumatology","volume":"38 2","pages":"Article 101980"},"PeriodicalIF":4.5,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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