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ID PMID Title PublicationDate abstract
32967052 Magnetic nanoparticles: A new diagnostic and treatment platform for rheumatoid arthritis. 2021 Feb Rheumatoid arthritis (RA) is a chronic inflammatory condition characterized by articular synovitis that eventually leads to the destruction of cartilage and bone in the joints with resulting pain and disability. The current therapies for RA are divided into 4 categories: non-steroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, nonbiological disease-modifying anti-rheumatic drugs (DMARDs), and biological DMARDs. Each drug grouping is beset with significant setbacks that not only include limited drug bioavailability and high clearance, but also varying degrees of drug toxicity to normal tissues. Recently, nanotechnology has provided a promising tool for the development of novel therapeutic and diagnostic systems in the area of malignant and inflammatory diseases. Among these, magnetic nanoparticles (MNPs) have provided an attractive carrier option for delivery of therapeutic agents. Armed with an extra magnetic probe, MNPs are capable of more accurately targeting the local lesion with avoidance of unpleasant systemic side effects. This review aims to provide an introduction to the applications of magnetic nanoparticles in RA, focusing on the latest advances, challenges, and opportunities for future development.
32524107 Trigger-responsive engineered-nanocarriers and image-guided theranostics for rheumatoid ar 2020 Jun 28 Rheumatoid Arthritis (RA), one of the leading causes of disability due to progressive autoimmune destruction of synovial joints, affects ∼1% of the global population. Standard therapy helps in reducing inflammation and delaying the progression of RA but is limited by non-responsiveness on long-term use and several side-effects. The conventional nanocarriers (CNCs), to some extent, minimize toxicity associated with free drug administration while improving the therapeutic efficacy. However, the uncontrolled release of the encapsulated drug even at off-targeted organs limits the application of CNCs. To overcome these challenges, trigger-responsive engineered nanocarriers (ENCs) have been recently explored for RA treatment. Unlike CNCs, ENCs enable precise control over on-demand drug release due to endogenous triggers in arthritic paws like pH, enzyme level, oxidative stress, or exogenously applied triggers like near-infrared light, magnetic field, ultrasonic waves, etc. As the trigger is selectively applied to the inflamed joint, it potentially reduces toxicity at off-target locations. Moreover, ENCs have been strategically coupled with imaging probe(s) for simultaneous monitoring of ENCs inside the body and facilitate an 'image-guided-co-trigger' for site-specific action in arthritic paws. In this review, the progress made in recently emerging 'trigger-responsive' and 'image-guided theranostics' ENCs for RA treatment has been explored with emphasis on the design strategies, mechanism, current status, challenges, and translational perspectives.
31211379 Arthritis self-efficacy beliefs and functioning among osteoarthritis and rheumatoid arthri 2020 May 1 OBJECTIVES: The Arthritis Self-Efficacy Scale (ASES) is a widely used self-report measure of beliefs reflecting confidence in one's capacity to function despite pain and control pain or other symptoms of arthritis. Despite evidence linking higher ASES scores to lower levels of impairment, pain and emotional distress, numerous modest, non-significant associations have also been observed. In this meta-analysis, we evaluated overall associations between ASES scores and adjustment in RA and OA samples as well as potential moderators that may explain the heterogeneity in these associations. METHOD: Data from 48 samples that met all 10 inclusion criteria (N = 9222 patients) were subject to analyses. RESULTS: ASES scores had significant medium average effect sizes with functional impairment, pain severity and emotional distress but substantial heterogeneity was evident for each association. ASES-impairment associations were moderated by the diagnosis, ASES version and ASES subscale content: significantly larger effect sizes were found for studies that included RA patients, used the original 20-item ASES and assessed subscale content reflecting the pursuit of daily activities despite pain (i.e. functional self-efficacy) than for studies based exclusively on OA patients, the eight-item ASES and ASES pain control and other symptom subscales. Relations of ASES scores with pain severity and emotional distress were moderated by ASES version and subscale content, respectively. CONCLUSION: The ASES has significant overall associations with key areas of functioning. Moderator analyses of the measure provide empirically grounded suggestions for optimal use of the ASES within OA and RA patient samples.
32739467 Exploring the therapeutic promise of targeting HMGB1 in rheumatoid arthritis. 2020 Oct 1 High mobility group box-1 (HMGB1) protein is a diverse, single polypeptide moiety, present in mammalian eukaryotic cells. In response to stimuli, this nuclear protein is actively secreted in to the extracellular compartment or passively released by the necrotic cells, in order to mediate inflammatory responses, by forming complexes with IL-1α, IL-1β, LPS and other moieties, and binding to RAGE, TLR and other receptor ligands, initiating downstream, signaling processes. This molecule acts as a proinflammatory cytokine and contributes to the progression of diseases like, acute lung injury, autoimmune liver damage, graft rejection immune response and arthritis. Small concentrations of HMGB1 are released during apoptosis, which facilitates oxidative regulation on Cys106, and propagates immune inactivating tolerogenic signals in the body. The review portrays the role of HMGB1 in rheumatoid arthritis, evidently supported by pre-clinical and clinical investigations, demonstrating extensive HMGB1 expression in synovial tissue and fluid as well as serum, excessive expression of transduction receptor signaling molecules, bone remodeling and uncontrolled expression of bone destroying osteoclastogenesis, resulting in destruction of articular cartilage, bone deformation and synovial proliferation, alleviating the pathogenesis in RA disease. Moreover, the review highlights the therapeutic regime targeting HMGB1, facilitating inhibition of its actions and release into the extracellular compartment, to ameliorate the destructive events that prevail in rheumatoid arthritis.
33301760 The prospects for targeting FcR as a novel therapeutic strategy in rheumatoid arthritis. 2021 Jan Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by synovial membrane hyperplasia, infiltration of inflammatory cells and bone tissue destruction. Although there have been many measures taken for RA therapy in recent years, they are not sufficiently safe or effective. Thus, it is very important to develop new drugs and slow down damage to other healthy organs in the case of RA. Lately, immunoglobulin Fc receptors (FcRs), such as the IgG Fc receptor (FcγR), IgA Fc receptor (FcαR), and IgD Fc receptor (FcδR), have been found to be involved in inducing or suppressing arthritis. FcRs interacting with immune complexes (ICs) are a key factor in the etiopathogenesis of RA. Therefore, an increasing number of methodsfor the targeted treatment of RA with FcRs are emerging, such as recombinant soluble FcγRs, recombinant multimeric Fc fragments and monoclonal antibodies, and have been demonstrated to significantly improve RA symptoms. Simultaneously, certain kinases involved in the downstream signaling of FcRs can also be a target for the treatment of RA, such as Syk and Btk inhibitors. An overview of these FcRs is provided in this review, including a description of FcR-related functions, signaling pathways, and potential FcR-targeting molecules for RA therapy. To date, the initial results of those developed FcR-targeting molecules have been promising. With this, FcRs might offer a better alternative to RA medication. Additionally, further pharmacological characterization and a better understanding of the unique mechanisms of FcR-targeting molecules are necessary.
32801037 Low-dose Interleukin-2: Biology and therapeutic prospects in rheumatoid arthritis. 2020 Oct Rheumatoid arthritis (RA) is a chronic aggressive arthritis that is characterized with systemic inflammation response, the production of abnormal antibodies, and persistent synovitis. One of the key mechanisms underlying the pathogenesis of RA is the imbalance of CD4 + T lymphocyte subsets, from T helper (Th) 17 cells and regulatory T (Treg) cells to T follicular helper (Tfh) cells and T follicular regulatory (Tfr) cells, which can mediate autoimmune inflammatory response to promote the overproduction of cytokines and abnormal antibodies. Although the treatment of RA has greatly changed due to the discovery of biological agents such as anti-TNF, the remission of it is still not satisfactory, thus, it is urgently required new treatment to realize the sustained remission of RA via restoring the immune tolerance. Interleukin-2 (IL-2) has been discovered to be a pleiotropic cytokine to promote inflammatory response and maintain immune tolerance. Low-dose IL-2 therapy is a driver of the imbalance between autoimmunity and immune tolerance towards immune tolerance, which has been tried to treat various autoimmune diseases. Recent researches show that low-dose IL-2 is a promising treatment for RA. In this review, we summarize the advances understandings in the biology of IL-2 and highlight the impact of the IL-2 pathway on the balance of Th17/Treg and Tfh/Tfr aiming to investigate the role of IL-2-mediated immune tolerance in RA and discuss the application and the therapeutic prospect of low-dose IL-2 in the treatment of RA.
32825059 Polymorphisms Involved in Response to Biological Agents Used in Rheumatoid Arthritis. 2020 Aug 19 Rheumatoid arthritis (RA) is a systemic disease that leads to joint destruction. During the last decade, the therapy of RA has been principally based on biological drugs. Although the efficacy of biological therapy has been established, patients demonstrated a high heterogeneity in clinical response to treatment. Several genetic polymorphisms play a part in the different response to biological drugs. This review summarizes the pharmacogenetics of biological agents approved for clinical RA treatment. We reviewed PubMed papers published over the past 20 years (2000-2020), inserting as the search term "rheumatoid arthritis and polymorphisms". Despite some studies showing important correlations between genetic polymorphisms and response to biological therapy in RA patients, most of these findings are still lacking and inconsistent. The personalized treatment according to a pharmacogenetics approach is promising but the available pharmacogenetics data on biological treatment in RA are not adequate and reliable to recommend pharmacogenetic tests before starting biological therapy in RA patients.
33327600 Biomarkers to Personalize the Treatment of Rheumatoid Arthritis: Focus on Autoantibodies a 2020 Dec 14 Rheumatoid arthritis (RA) is a chronic inflammatory disease that is very complex and heterogeneous. If not adequately treated, RA patients are likely to manifest excess of morbidity and disability with an important impact on the quality of life. Pharmacological treatment is based on the administration of the disease-modifying antirheumatic drugs (DMARDs), subdivided into conventional synthetic (csDMARDs), targeted synthetic (tsDMARDs), and biological (bDMARDs). bDMARDs are now frequently administered in patients, both as alternative treatment and together with csDMARDs. Unfortunately, there is a therapeutic response variability both to old and new drugs. Therefore, to identify pre-therapeutic and on-treatment predictors of response is a priority. This review aims to summarize recent advances in understanding the causes of the variability in treatment response in RA, with particular attention to predictive potential of autoantibodies and DMARD pharmacogenetics. In recent years, several biomarkers have been proposed to personalize the therapy. Unfortunately, a magic bullet does not exist, as many factors concur to disease susceptibility and treatment outcomes, acting around the patient's congenital background. Models integrating demographic, clinical, biochemical, and genetic data are needed to enhance the predictive capacity of specific factors singularly considered to optimize RA treatment in light of multidisciplinary patient management.
33215529 LncRNA GAS5 alleviates rheumatoid arthritis through regulating miR-222-3p/Sirt1 signalling 2021 Feb INTRODUCTION: Rheumatoid arthritis (RA) is an autoimmune disease that affects millions of people. Fibroblast-like synoviocytes (FLSs) located in rheumatoid panni play a pivotal role in the formation of RA. The long noncoding RNA (lncRNA) GAS5 is reportedly downregulated in rheumatoid arthritis. However, its detailed mechanism in RA remains to be explored. This study investigated the roles and related mechanisms of GAS5 in RA. METHODS: The expression levels of GAS5, miR-222-3p, and sirtuin 1 (Sirt1) were evaluated by quantitative PCR (qPCR). Cell proliferation was analyzed by CCK-8 and BrdU assays. Cell apoptosis was assessed by flow cytometry and western blotting. Enzyme-linked immunosorbent assay (ELISA) was utilized to evaluate the levels of TNF-α, IL-1β, and IL-6. The interaction between GAS5 or Sirt1 and miR-222-3p was predicted by starBase and validated by dual-luciferase reporter assay. RESULTS: GAS5 expression was found to be downregulated in the serum samples of RA patients and in RA-FLSs. GAS5 overexpression or the inhibition of miR-222-3p impeded the activity of RA-FLSs by repressing their proliferation and inflammation and by promoting apoptosis. Mechanistically, GAS5 indirectly regulates Sirt1 expression by binding miR-222-3p. Further experiments confirmed that Sirt1 overexpression restored the anti-RA activity of GAS5 under miR-222-3p mimic. CONCLUSIONS: The miR-222-3p/Sirt1 axis was found to be critical for the function of GAS5 in regulating the proliferation, inflammation, and apoptosis of RA-FLSs. These data indicate GAS5 activation as a potential therapeutic strategy for RA progression.
32635779 Adoptive Treg cell-based immunotherapy: Frontier therapeutic aspects in rheumatoid arthrit 2020 Aug The major current focus on treating rheumatoid arthritis is to put an end to long-term treatments and instead, specifically block widespread immunosuppression by developing antigen-specific tolerance, while also permitting an intact immune response toward other antigens to occur. There have been promising preclinical findings regarding adoptive Treg cells immunotherapy with a critically responsible function in the prevention of autoimmunity, tissue repair and regeneration, which make them an attractive candidate to develop effective therapeutic approaches to achieve this interesting concept in many human immune-mediated diseases, such as rheumatoid arthritis. Ex vivo or invivo manipulation protocols are not only utilized to correct Treg cells defect, but also to benefit from their specific immunosuppressive properties by identifying specific antigens that are expressed in the inflamedjoint. The methods able to address these deficiencies can be considered as a target for immunity interventions to restore appropriate immune function.
33260629 Effects of Biological Therapies on Molecular Features of Rheumatoid Arthritis. 2020 Nov 28 Rheumatoid arthritis (RA) is an autoimmune and chronic inflammatory disease primarily affecting the joints, and closely related to specific autoantibodies that mostly target modified self-epitopes. Relevant findings in the field of RA pathogenesis have been described. In particular, new insights come from studies on synovial fibroblasts and cells belonging to the innate and adaptive immune system, which documented the aberrant production of inflammatory mediators, oxidative stress and NETosis, along with relevant alterations of the genome and on the regulatory epigenetic mechanisms. In recent years, the advances in the understanding of RA pathogenesis by identifying key cells and cytokines allowed the development of new targeted disease-modifying antirheumatic drugs (DMARDs). These drugs considerably improved treatment outcomes for the majority of patients. Moreover, numerous studies demonstrated that the pharmacological therapy with biologic DMARDs (bDMARDs) promotes, in parallel to their clinical efficacy, significant improvement in all these altered molecular mechanisms. Thus, continuous updating of the knowledge of molecular processes associated with the pathogenesis of RA, and on the specific effects of bDMARDs in the correction of their dysregulation, are essential in the early and correct approach to the treatment of this complex autoimmune disorder. The present review details basic mechanisms related to the physiopathology of RA, along with the core mechanisms of response to bDMARDs.
31984496 Rheumatoid arthritis and periodontitis in adults: Using the Korean National Health Insuran 2020 Sep BACKGROUND: Using the database of the National Health Insurance Service-National Sample Cohort (NHIS-NSC), we aimed to assess the relationship between the prevalence of rheumatoid arthritis (RA) and periodontitis. METHODS: Participants aged ≥19 years with a previous health check-up at the NHIS between 2009 and 2015 were selected. In total, 559,280 participants were included after implementing appropriate exclusion criteria. The Chi-squared test was used to compare the general and health-related characteristics of participants with and without RA or periodontitis. Univariate and multivariate logistic regression analyses with consecutive adjustment for confounders, were used to assess the association between the prevalence of rheumatoid arthritis and periodontitis. RESULTS: The prevalence of rheumatoid arthritis in patients with and without periodontitis was 6.2% and 5.2%, respectively. The prevalence of periodontitis in patients with and without rheumatoid arthritis was 19.6% and 16.6%, respectively. The possibility of having rheumatoid arthritis was greater in patients with periodontitis than in individuals without periodontitis (odds ratio [OR]; 1.22, P <0.001), and remained high (OR; 1.07, P <0.001) after adjusting for confounders. CONCLUSION: Our results revealed a significant association between the prevalence of rheumatoid arthritis and periodontitis.
31644463 Evolving concepts of the pathogenesis of rheumatoid arthritis with focus on the early and 2020 Jan PURPOSE OF REVIEW: To provide an overview of recently published work covering key mechanisms involved in the pathogenesis of rheumatoid arthritis (RA), with focus on the early and late stages. RECENT FINDINGS: Present understanding of RA pathogenesis has been mainly focused on the inflammatory process at the established phase of the disease, but recent work has shed light on important molecular and cellular mechanisms involved both at the early and late/refractory stages. In early RA, the involvement of anticitrullinated protein antibodies in RA induction has been identified with a critical role of the IL-23/Th17 axis in the control of their pathogenicity. At the late stage, RA may be viewed as a cell-autonomous genetic and epigenetic disease, characterized by altered cell death pathways in synoviocytes after long-term exposure to inflammation. An improved knowledge of these cell-intrinsic altered pathways is the basis for the targeting of pathogenic synoviocytes, as a new therapeutic alternative against resistance to current treatment targeting the immune system. SUMMARY: We summarize these pathological pathways, and their understanding will facilitate the design of new diagnostic tools and therapeutic strategies combining the targeting of pathogenic synoviocytes with current immune-targeted therapies.
32176395 The importance of differences; On environment and its interactions with genes and immunity 2020 May The current review uses rheumatoid arthritis (RA) as a prominent example for how studies on the interplay between environmental and genetic factors in defined subsets of a disease can be used to formulate aetiological hypotheses that subsequently can be tested for causality using molecular and functional studies. Major discussed findings are that exposures to airways from many different noxious agents including cigarette smoke, silica dust and more interact with major susceptibility genes, mainly HLA-DR genetic variants in triggering antigen-specific immune reactions specific for RA. We also discuss how several other environmental and lifestyle factors, including microbial, neural and metabolic factors, can influence risk for RA in ways that are different in different subsets of RA.The description of these processes in RA provides the best example so far in any immune-mediated disease of how triggering of immunity at one anatomical site in the context of known environmental and genetic factors subsequently can lead to symptoms that precede the classical inflammatory disease symptoms and later contribute also to the classical RA joint inflammation. The findings referred to in the review have led to a change of paradigms for very early therapy and prevention of RA and to efforts towards what we have named 'personalized prevention'. We believe that the progress described here for RA will be of relevance for research and practice also in other immune-mediated diseases.
32571398 Modifiable environmental exposure and risk of rheumatoid arthritis-current evidence from g 2020 Jun 22 Rheumatoid arthritis (RA) is a multifactorial chronic autoimmune disease, which involves a complex interplay of environmental triggers and genetic components in its etiology. It has been shown that genetics only explain about half of the liability to develop RA, leaving a large room for non-genetic factors. Indeed, several environmental exposures including smoking, drinking, obesity, and dietary patterns (and more) have been identified to be associated with RA risk, yet the observational nature of conventional epidemiological investigation hampers causal inference, as the validity of results could be plagued by measurement error, confounding, and/or reverse causality. Mendelian randomization (MR) is a novel statistical approach that uses genetic variants as instrumental variables (IV) to make causal inferences from observational data. The current genetic discoveries in the many heritable and modifiable human complex traits have provided an exceptional opportunity to evaluate a putative causal relationship between exposure and outcome in the absence of high-quality experimental or intervention studies, through a MR design. In the current review, we detail the contribution of MR studies hitherto conducted for modifiable environmental exposures with the risk of RA to understand the role of these factors in RA pathogenesis. We start with a brief introduction of each study, follow by a summarization of shortcomings and conclude by highlighting future directions. The application of MR design in the field of rheumatology remains limited. Only a few MR studies have examined the causal roles of vitamin D, cigarette smoking, alcohol consumption, coffee consumption, and levels of education in RA, where, no consistent evidence for a causal relationship has been found. Most studies lacked sensitivity analyses to verify MR model assumptions and to guarantee the validity of results. Almost all studies are likely to bias the strength of association towards a null value, since they used IVs from earlier GWAS(s) of exposures with a small sample size (i.e., few genetic markers). As the magnitudes of GWAS expand rapidly, additional trait-associated loci have been discovered. Incorporating these loci would greatly improve the strength of genetic instruments, as well as both the accuracy and precision of MR estimates. To conclude, there is a need for an update and a huge space for improvement of future MR studies in RA.
32338187 New insights into IFN-γ in rheumatoid arthritis: role in the era of JAK inhibitors. 2020 Jun The treatment of rheumatoid arthritis (RA) is now entering a new era, the era of Janus kinase (JAK) inhibitors. JAK inhibitors target multiple cytokines including IL-6 and exhibit a beneficial treatment effect in patients with RA and inadequate response to conventional synthetic or biologic disease-modifying anti-rheumatic drugs. Since the treatment effect of JAK inhibitors is promising even for patients refractory to anti-IL-6 therapy, it needs to be considered how multiple cytokines play roles in the pathogenesis of RA. It is also worth noting that an increased risk of herpes zoster is specifically related to the use of JAK inhibitors. Among cytokines targeted by JAK inhibitors, the current review focuses on IFN-γ, particularly on its role in synovial biology, autoimmunity, bone metabolism, pain, and varicella zoster virus infection. Recent studies provided new insights into IFN-γ in the pathogenesis of RA, which may account for the efficacy of JAK inhibitors.
32035199 Rheumatoid Meningitis. 2020 May BACKGROUND: Rheumatoid meningitis is a rare manifestation of autoimmune rheumatoid arthritis. CASE DESCRIPTION: A 70-year-old man with rheumatoid arthritis had presented with speech difficulties and limb weakness. Magnetic resonance imaging of his brain demonstrated diffuse meningeal enhancement. A biopsy confirmed the presence of rheumatoid meningitis. CONCLUSION: In the present report, we have discussed the diagnostic and therapeutic approach to rheumatoid meningitis.
31899021 Prevention and cure: The major unmet needs in the management of rheumatoid arthritis. 2020 Jun The outcome of treatment of patients with rheumatoid arthritis (RA) has qualitatively improved in recent years due to better and earlier treatment approaches, and new drugs. It is now generally accepted that the phenotype of RA is the end-point of a disease continuum. Large retrospective studies have identified anti-citrullinated protein antibodies (ACPAs) and rheumatoid factor in the stored serum of patients, years before the development of clinical RA. Recent data suggest mucosal sites such as the oral mucosa (in particular the periodontium), lung and gut may be the sites where auto-immunity is initiated. The role of bacteria at these sites is reviewed. Much recent work has focussed on the role of high resolution imaging namely ultrasound and magnetic resonance imaging in identifying subclinical inflammation in at-risk individuals with early musculoskeletal symptoms (e.g. arthralgia) but without clinical synovitis. Importantly, the first musculoskeletal site involved is usually not the joint (synovium). Sub-clinical disease predicts the onset of clinical arthritis, and its timing, in symptomatic at-risk individuals. These and other predictive markers will be described. The ability to identify patients at-risk of RA before joint involvement has led to interventions aimed at preventing/delaying disease. Once arthritis occurs, rapid remission is the target of therapy. The percentage of patients with RA achieving clinical remission has improved markedly compared with a few decades ago. The optimum outcome is to induce remission sufficiently profound so that therapy can be stopped, without flare, that is drug-free remission, which is effectively cure. Limitations of the tools used to measure remission, the outcome of tapering therapy, and new approaches to achieve successful drug cessation are described. Overall, this article reviews progress towards meeting the unmet needs of prevention/cure.
33396685 The Role of Nutritional Factors and Intestinal Microbiota in Rheumatoid Arthritis Developm 2020 Dec 30 Evidence about the role of nutritional factors and microbiota in autoimmune diseases, and in rheumatoid arthritis (RA) in particular, has grown in recent years, however many controversies remain. The aim of this review is to summarize the role of nutrition and of the intestinal microbiota in the development of RA. We will focus on selected dietary patterns, individual foods and beverages that have been most consistently associated with RA or with the occurrence of systemic autoimmunity associated with RA. We will also review the evidence for a role of the intestinal microbiota in RA development. We propose that diet and digestive microbiota should be considered together in research, as they interact and may both be the target for future preventive interventions in RA.
32007647 Bronchiectasis in rheumatoid arthritis. A clinical appraisial. 2020 Oct Bronchiectasis is defined as irreversibly damaged and dilated bronchi and is one of the most common pulmonary manifestations in patients with rheumatoid arthritis (RA). The model of RA-associated autoimmunity induced in some individuals by chronic bacterial infection in bronchiectasis is becoming increasingly acceptable, although a genetic predisposition to RA-associated bronchiectasis has also been demonstrated. Bronchiectasis should be suspected in RA patients with chronic cough and sputum production or frequent respiratory infections and the diagnosis must be confirmed by thoracic high-resolution computed tomography. Management of patients with RA-associated bronchiectasis includes a multimodal treatment approach. Similar to all patients with non-cystic fibrosis bronchiectasis, patients with RA-associated bronchiectasis benefit from a pulmonary rehabilitation program, including an exercise/muscle strengthening program and an education program with a specific session on airway clearance techniques. Prophylactic antibiotics are recommended for patients with frequent (3 or more infective exacerbations per year) or severe infections requiring hospitalization/intravenous antibiotics and inhaled corticosteroids and long-acting β2-agonists should be used in patients with non-cystic fibrosis bronchiectasis and associated airway hyper-responsiveness. In patients with RA-associated bronchiectasis the use of immunomodulatory drugs has to be carefully considered, as they are essential to control disease activity, despite being associated with an increased infectious risk. Pneumococcal and influenza vaccines are advised to all patients with RA-associated bronchiectasis in order to reduce the risk of infection. Patients with RA-associated bronchiectasis have a poorer prognosis than those with either RA or bronchiectasis alone and require regular follow-up, under the joint care of a rheumatologist and a pulmonologist.