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Mysteries of kidney-protecting parasitic infection revealed
Joanna Clarke
doi : 10.1038/s41584-021-00655-6
Nature Reviews Rheumatology volume 17, page441 (2021)
Targeting the CCR6–CCL20 axis improves experimental PsA
Sarah Onuora
doi : 10.1038/s41584-021-00663-6
Nature Reviews Rheumatology volume 17, page441 (2021)
AAV remission possible with reduced steroid dose
Joanna Clarke
doi : 10.1038/s41584-021-00658-3
Nature Reviews Rheumatology volume 17, page442 (2021)
Rituximab shows promise for skin disease in SSc
Joanna Clarke
doi : 10.1038/s41584-021-00659-2
Nature Reviews Rheumatology volume 17, page442 (2021)
B cell X-chromosome inactivation is faulty in SLE
Joanna Clarke
doi : 10.1038/s41584-021-00660-9
Nature Reviews Rheumatology volume 17, page442 (2021)
Molecular classification divides pSS into 4 groups
Joanna Clarke
doi : 10.1038/s41584-021-00661-8
Nature Reviews Rheumatology volume 17, page442 (2021)
Synthetic Wnt agonists rapidly rebuild bone in vivo
Sarah Onuora
doi : 10.1038/s41584-021-00664-5
Nature Reviews Rheumatology volume 17, page442 (2021)
Modifying exosomes to target macrophages in arthritis
Jessica McHugh
doi : 10.1038/s41584-021-00651-w
Nature Reviews Rheumatology volume 17, page443 (2021)
Tumour protein linked to FLS phenotype in RA
Gabriella Szylar
doi : 10.1038/s41584-021-00662-7
Nature Reviews Rheumatology volume 17, page443 (2021)
Targeting calcium-related mechanotransduction in early OA
Michelle L. Delco & Lawrence J. Bonassar
doi : 10.1038/s41584-021-00649-4
Nature Reviews Rheumatology volume 17, pages445–446 (2021)
Rheumatology resources need reform to represent all patients
Lisa Zickuhr & Heather A. Jones
doi : 10.1038/s41584-021-00636-9
Nature Reviews Rheumatology volume 17, pages447–448 (2021)
Lyme arthritis: linking infection, inflammation and autoimmunity
Robert B. Lochhead, Klemen Strle, Sheila L. Arvikar, Janis J. Weis & Allen C. Steere
doi : 10.1038/s41584-021-00648-5
Nature Reviews Rheumatology volume 17, pages449–461 (2021)
Infectious agents can trigger autoimmune responses in a number of chronic inflammatory diseases. Lyme arthritis, which is caused by the tick-transmitted spirochaete Borrelia burgdorferi, is effectively treated in most patients with antibiotic therapy; however, in a subset of patients, arthritis can persist and worsen after the spirochaete has been killed (known as post-infectious Lyme arthritis). This Review details the current understanding of the pathogenetic events in Lyme arthritis, from initial infection in the skin, through infection of the joints, to post-infectious chronic inflammatory arthritis. The central feature of post-infectious Lyme arthritis is an excessive, dysregulated pro-inflammatory immune response during the infection phase that persists into the post-infectious period. This response is characterized by high amounts of IFN? and inadequate amounts of the anti-inflammatory cytokine IL-10. The consequences of this dysregulated pro-inflammatory response in the synovium include impaired tissue repair, vascular damage, autoimmune and cytotoxic processes, and fibroblast proliferation and fibrosis. These synovial characteristics are similar to those in other chronic inflammatory arthritides, including rheumatoid arthritis. Thus, post-infectious Lyme arthritis provides a model for other chronic autoimmune or autoinflammatory arthritides in which complex immune responses can be triggered and shaped by an infectious agent in concert with host genetic factors.
Genome editing to define the function of risk loci and variants in rheumatic disease
Yuriy Baglaenko, Dana Macfarlane, Alexander Marson, Peter A. Nigrovic & Soumya Raychaudhuri
doi : 10.1038/s41584-021-00637-8
Nature Reviews Rheumatology volume 17, pages462–474 (2021)
Discoveries in human genetic studies have revolutionized our understanding of complex rheumatic and autoimmune diseases, including the identification of hundreds of genetic loci and single nucleotide polymorphisms that potentially predispose individuals to disease. However, in most cases, the exact disease-causing variants and their mechanisms of action remain unresolved. Functional follow-up of these findings is most challenging for genomic variants that are in non-coding genomic regions, where the large majority of common disease-associated variants are located, and/or that probably affect disease progression via cell type-specific gene regulation. To deliver on the therapeutic promise of human genetic studies, defining the mechanisms of action of these alleles is essential. Genome editing technology, such as CRISPR–Cas, has created a vast toolbox for targeted genetic and epigenetic modifications that presents unprecedented opportunities to decipher disease-causing loci, genes and variants in autoimmunity. In this Review, we discuss the past 5–10 years of progress in resolving the mechanisms underlying rheumatic disease-associated alleles, with an emphasis on how genomic editing techniques can enable targeted dissection and mechanistic studies of causal autoimmune risk variants.
Current and future therapies for primary Sj?gren syndrome
Raphaèle Seror, Gaetane Nocturne & Xavier Mariette
doi : 10.1038/s41584-021-00634-x
Nature Reviews Rheumatology volume 17, pages475–486 (2021)
Primary Sj?gren syndrome (pSS) is a systemic autoimmune disease that is characterized by a triad of symptoms that affect all patients (dryness, pain and fatigue). In addition, systemic involvement can affect between one-third and one-half of patients. The management of patients with pSS has been negatively affected by a lack of effective treatments; however, knowledge of the epidemiology of pSS has increased, and advances in developing classification criteria, systemic disease activity scoring and patient-reported outcomes have been made during the past decade. Progress has also been made in understanding the mechanisms that underlie the pathogenesis of pSS, which has enabled a more targeted therapeutic approach to be taken. At present, therapeutic decisions rely on the evaluation of symptoms and systemic manifestations and are mostly formed on the basis of experience rather than evidence, and on similarities with other autoimmune diseases, although the 2019 management recommendations from EULAR are now being used to inform clinical management of pSS. This Review summarizes the available evidence for systemic treatments for pSS and includes discussions of advances in outcome assessment, the current evidence for DMARD use and an overview of promising future therapeutics.
Insights into the biology and therapeutic implications of TNF and regulatory T cells
Benoit L. Salomon
doi : 10.1038/s41584-021-00639-6
Nature Reviews Rheumatology volume 17, pages487–504 (2021)
Treatments that block tumour necrosis factor (TNF) have major beneficial effects in several autoimmune and rheumatic diseases, including rheumatoid arthritis. However, some patients do not respond to TNF inhibitor treatment and rare occurrences of paradoxical disease exacerbation have been reported. These limitations on the clinical efficacy of TNF inhibitors can be explained by the differences between TNF receptor 1 (TNFR1) and TNFR2 signalling and by the diverse effects of TNF on multiple immune cells, including FOXP3+ regulatory T cells. This basic knowledge sheds light on the consequences of TNF inhibitor therapies on regulatory T cells in treated patients and on the limitations of such treatment in the control of diseases with an autoimmune component. Accordingly, the next generation of drugs targeting TNF is likely to be based on agents that selectively block the binding of TNF to TNFR1 and on TNFR2 agonists. These approaches could improve the treatment of rheumatic diseases in the future.
TNF inhibition for immune checkpoint inhibitor-induced irAEs: the jury is still out
Karijn P. M. Suijkerbuijk & Rik J. Verheijden
doi : 10.1038/s41584-021-00640-z
Nature Reviews Rheumatology volume 17, page505 (2021)
Reply to: TNF inhibition for immune checkpoint inhibitor-induced irAEs: the jury is still out
Anne R. Bass & Allen Y. Chen
doi : 10.1038/s41584-021-00641-y
Nature Reviews Rheumatology volume 17, pages505–506 (2021)
