Kenneth G. Saag
doi : 10.1002/art.42475
Flavia Sunzini, Andrew Schrepf, Daniel J. Clauw, Neil Basu
doi : 10.1002/art.42429
Chronic pain is a major socioeconomic burden globally. The most frequent origin of chronic pain is musculoskeletal. In inflammatory musculoskeletal diseases such as rheumatoid arthritis (RA), chronic pain is a primary determinant of deleterious quality of life. The pivotal role of peripheral inflammation in the initiation and perpetuation of nociceptive pain is well-established among patients with musculoskeletal diseases.
Shirkhan Amikishiyev, M. Guven Gunver, Murat Bektas, Sarvan Aghamuradov, Burak Ince, Nevzat Koca, Ege Sinan Torun, Numune Aliyeva, Selma Sari, Cigdem Cetin, Banu C. Yalcin-Dulundu, Rabia Deniz, Fatih Kemik, Besim Fazil Agargun, Ubeyde Ayse Gulseren, Beliz Besisik, Onur Alkan, Ceren Bagriacik, Yavuz B. Tor, Naci Senkal, Yunus Catma, Gorkem Durak, Sevim Mese, Ali Agacfidan, Murat Kose, Mustafa Erelel, A. Atahan Cagatay, Serap Simsek-Yavuz, Sevgi Kalayoglu-Besisik, Figen Esen, Ahmet Gül
doi : 10.1002/art.42417
Hyperinflammation (HI) that develops in week 2 of COVID-19 contributes to a worse outcome. Because week 2 laboratory findings can be relatively mild, the available criteria for classification of hemophagocytic lymphohistiocytosis or macrophage activation syndrome are not helpful.
Sara Turcinov, Erik af Klint, Bertrand Van Schoubroeck, Arlette Kouwenhoven, Sohel Mia, Karine Chemin, Hans Wils, Carl Van Hove, An De Bondt, Ken Keustermans, Jeroen Van Houdt, Joke Reumers, Nathan Felix, Navin L. Rao, Pieter Peeters, Frederik Stevenaert, Lars Klareskog, Murray McKinnon, Daniel Baker, Anish Suri, Vivianne Malmström
doi : 10.1002/art.42407
CD4+ T cells are implicated in rheumatoid arthritis (RA) pathology from the strong association between RA and certain HLA class II gene variants. This study was undertaken to examine the synovial T cell receptor (TCR) repertoire, T cell phenotypes, and T cell specificities in small joints of RA patients at time of diagnosis before therapeutic intervention.
Luigi Del Sordo, Garth B. Blackler, Holly T. Philpott, Jared Riviere, Lakshman Gunaratnam, Bryan Heit, C. Thomas Appleton
doi : 10.1002/art.42412
Osteoarthritis (OA) exposes all joint tissues to physiologic stresses, increasing the need to clear apoptotic cells from tissues, including the synovium. We undertook this study to assess the burden of apoptotic cells in synovial tissue in patients with late-stage knee OA and to investigate whether OA impairs the macrophage-mediated clearance of apoptotic cells via efferocytosis.
Lucy M. Carter, Adewonuola Alase, Zoe Wigston, Antonios Psarras, Agata Burska, Emily Sutton, Md Yuzaiful Md Yusof, John A. Reynolds, The MASTERPLANS Consortium, Neil McHugh, Paul Emery, Miriam Wittmann, Ian N. Bruce, Edward M. Vital
doi : 10.1002/art.42404
Gene expression profiles are associated with the clinical heterogeneity of systemic lupus erythematosus (SLE) but are not well studied as biomarkers for therapy. We studied gene expression and response to rituximab in a multiethnic UK cohort who were refractory to standard therapy.
Hanane El Bannoudi, MacIntosh Cornwell, Elliot Luttrell-Williams, Alexis Engel, Christina Rolling, Tessa J. Barrett, Peter Izmirly, H. Michael Belmont, Kelly Ruggles, Robert Clancy, Jill Buyon, Jeffrey S. Berger
doi : 10.1002/art.42382
Platelets are mediators of inflammation with immune effector cell properties and have been implicated in the pathogenesis of systemic lupus erythematosus (SLE).
Melissa E. Munroe, Derek Blankenship, Daniele DeFreese, Mohan Purushothaman, Wade DeJager, Susan Macwana, Joel M. Guthridge, Stan Kamp, Nancy Redinger, Teresa Aberle, Eliza F. Chakravarty, Cristina Arriens, Yanfeng Li, Hu Zeng, Kathleen A. McCarthy-Fruin, Shirley-Ann Osei-Onomahm, Uma Thanarajasingam, Judith A. James, Eldon Jupe
doi : 10.1002/art.42389
Systemic lupus erythematosus (SLE) is marked by immune dysregulation linked to varied clinical disease activity. Using a unique longitudinal cohort of SLE patients, this study sought to identify optimal immune mediators informing an empirically refined flare risk index (FRI) reflecting altered immunity prior to clinical disease flare.
Alvise Berti, Sophie Hillion, Maximilian F. Konig, Marta Casal Moura, Amber M. Hummel, Eva Carmona, Tobias Peikert, Fernando C. Fervenza, Cees G.M. Kallenberg, Carol A. Langford, Peter A. Merkel, Paul A. Monach, Philip Seo, Robert F. Spiera, Paul Brunetta, E. William St. Clair, Kristina M. Harris, John H. Stone, Guido Grandi, Jacques-Olivier Pers, Ulrich Specks, Divi Cornec
doi : 10.1002/art.42388
Autoreactive B cells are responsible for antineutrophil cytoplasmic antibody (ANCA) production in ANCA-associated vasculitis (AAV). Rituximab (RTX) depletes circulating B cells, including autoreactive B cells. We aimed to evaluate changes and associations with relapse of the circulating autoreactive B cell pool following therapeutic B cell depletion in AAV.
Marta Casal Moura, Gwen E. Thompson, Darlene R. Nelson, Lynn A. Fussner, Amber M. Hummel, Dieter E. Jenne, Daniel Emerling, Fernando C. Fervenza, Cees G. M. Kallenberg, Carol A. Langford, W. Joseph McCune, Peter A. Merkel, Paul A. Monach, Philip Seo, Robert F. Spiera, E. William St. Clair, Steven R. Ytterberg, John H. Stone, William H. Robinson, Ulrich Specks
doi : 10.1002/art.42418
Proteinase 3 (PR3) is the major antigen for antineutrophil cytoplasmic antibodies (ANCAs) in the systemic autoimmune vasculitis, granulomatosis with polyangiitis (GPA). PR3-targeting ANCAs (PR3-ANCAs) recognize different epitopes on PR3. This study was undertaken to study the effect of mutations on PR3 antigenicity.
Sebastian Klapa, Antje Müller, Andreas Koch, Anja Kerstein-Stähle, Wataru Kähler, Harald Heidecke, Susanne Schinke, Markus Huber-Lang, Martin Nitschke, Silke Pitann, Solveig Augustin, Christian M. Karsten, Gabriela Riemekasten, Peter Lamprecht
doi : 10.1002/art.42410
To examine concentrations of circulating antibodies targeting C3a and C5a complement receptors in antineutrophil cytoplasmic autoantibody (ANCA)–associated vasculitis (AAV) and analyze their association with disease activity.
Alexandru-Emil Matei, Markéta Kubánková, Liyan Xu, Andrea-Hermina Györfi, Evgenia Boxberger, Despina Soteriou, Maria Papava, Julia Prater, Xuezhi Hong, Christina Bergmann, Martin Kräter, Georg Schett, Jochen Guck, Jörg H. W. Distler
doi : 10.1002/art.42394
Pathologically activated circulating immune cells, including monocytes, play major roles in systemic sclerosis (SSc). Their functional characterization can provide crucial information with direct clinical relevance. However, tools for the evaluation of pathologic immune cell activation and, in general, of clinical outcomes in SSc are scarce.
David Ordóñez, Robert B. Lochhead, Klemen Strle, Annalisa Pianta, Sheila Arvikar, Ildiko Van Rhijn, Anat Stemmer-Rachamimov, Allen C. Steere
doi : 10.1002/art.42408
Obliterative microvascular lesions are found in the synovial tissue of ~50% of patients with post-antibiotic Lyme arthritis (LA) and correlate with autoantibodies to certain vascular antigens. In this study, we identified lymphocytes with cytotoxic potential that may also mediate this feature of synovial pathology.
Khaled Elsaid, Tony R. Merriman, Leigh-Ana Rossitto, Ru Liu-Bryan, Jacob Karsh, Amanda Phipps-Green, Gregory D. Jay, Sandy Elsayed, Marwa Qadri, Marin Miner, Murray Cadzow, Talia J. Dambruoso, Tannin A. Schmidt, Nicola Dalbeth, Ashika Chhana, Jennifer Höglund, Majid Ghassemian, Anaamika Campeau, Nancy Maltez, Niclas G. Karlsson, David J. Gonzalez, Robert Terkeltaub
doi : 10.1002/art.42413
In gout, hyperuricemia promotes urate crystal deposition, which stimulates the NLRP3 inflammasome and interleukin-1β (IL-1β)–mediated arthritis. Incident gout without background hyperuricemia is rarely reported.
Yeonghee Eun, Kyungdo Han, Seung Woo Lee, Kyunga Kim, Seonyoung Kang, Seulkee Lee, Hoon-Suk Cha, Eun-Mi Koh, Hyungjin Kim, Jaejoon Lee
doi : 10.1002/art.42381
Few data are available on whether changes in metabolic syndrome affect incident gout. This study was undertaken to assess associations between metabolic syndrome status and incident gout, as well as changes in the clinical characteristics of metabolic syndrome and incident gout, in a cohort of young men.
Nicholas A. Sumpter, Riku Takei, Murray Cadzow, Ruth K. G. Topless, Amanda J. Phipps-Green, Rinki Murphy, Janak de Zoysa, Huti Watson, Muhammad Qasim, Alexa S. Lupi, Abhishek Abhishek, Mariano Andrés, Tania O. Crișan, Michael Doherty, Lennart Jacobsson, Matthijs Janssen, Tim L. Jansen, Leo A. B. Joosten, Meliha Kapetanovic, Frédéric Lioté, Hirotaka Matsuo, Geraldine M. McCarthy, Fernando Perez-Ruiz, Philip Riches, Pascal Richette, Edward Roddy, Blanka Stiburkova, Alexander So, Anne-Kathrin Tausche, Rosa J. Torres, Till Uhlig, Tanya J. Major, Lisa K. Stamp, Nicola Dalbeth, Hyon K. Choi, Ana I. Vazquez, Megan P. Leask, Richard J. Reynolds, Tony R. Merriman
doi : 10.1002/art.42393
To determine whether a gout polygenic risk score (PRS) is associated with age at gout onset and tophaceous disease in European, East Polynesian, and West Polynesian men and women with gout.
Julia Kuehn, Susanne Schleifenbaum, Michaela Hendling, Sandra Siebenhandl, Julie Krainer, Sabrina Fuehner, Antje Hellige, Carolin Park, Claas Hinze, Helmut Wittkowski, Dirk Holzinger, Lorenz Thurner, Andreas Weinhäusel, Dirk Foell, Christoph Kessel
doi : 10.1002/art.42409
Systemic juvenile idiopathic arthritis (JIA) features characteristics of autoinflammation and autoimmunity, culminating in chronic arthritis. In this study, we hypothesized that aberrant or incomplete polarization of T helper cells contributes to disease pathology.
Jiayu Meng, Na Li, Xianyang Liu, Shengjun Qiao, Qian Zhou, Jun Tan, Ting Zhang, Zhifang Dong, Xiaopeng Qi, Aize Kijlstra, Liming Mao, Peizeng Yang, Shengping Hou
doi : 10.1002/art.42420
The NLRP3 inflammasome has been shown to be involved in the development of uveitis, but the exact mechanism remains elusive. This study was undertaken to explore the role of NLRP3 in the development of uveitis.
Mariele Gatto, Sara Bjursten, Charlotte A. Jonsson, Monica Leu Agelii, Caroline Jonell, Sarah McGrath, Erik Lönnblom, Outi Sareila, Rikard Holmdahl, Anna Rudin, Max Levin, Inger Gjertsson
doi : 10.1002/art.42406
To investigate potential associations between B cell–related immunologic changes and development of inflammatory arthritis (IA) after treatment with immune checkpoint inhibitors (ICIs).
Jerney de Jongh, Gerben J. C. Zwezerijnen, Maqsood Yaqub, Conny J. van der Laken
doi : 10.1002/art.42400
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