Results 181 to 190 of about 1,101,865 (283)
Cancer in Systemic Sclerosis: Clinical Associations and Prognostic Impact From the EUSTAR Registry
Arthritis &Rheumatology, EarlyView.Objective
Cancer represents a major cause of death in systemic sclerosis (SSc). Established risk factors are limited to specific subsets, particularly early diffuse anti‐RNA polymerase III (POLR3)–positive disease, needing further exploration. Methods
We performed a nested case‐control study within the European Scleroderma Trials and Research group ...Antonio Tonutti, Francesca Motta, Liala Moschetti, Cosimo Bruni, Carina Mihai, Claudia Iannone, Maria Rosa Pellico, Stefano Stano, Stefano Erba, Claudia Barison, Eleonora Pazzi, Andrea Benini, Beatrice Moccaldi, Kurszán Jász Dávid, Ágnes Ágoston‐Szabó, Beatrice Gabrielli, Francesca Nava, Dóra Tari, Francesca Romana Di Ciommo, Yuri Sasaki, Gonçalo Boleto, Radim Bečvář, Alejandro Brigante, Britta Maurer, Massimiliano Limonta, Rahma A. Elziaty, Fabiola Atzeni, Lilian Maria López Núñez, Roberta Foti, Francesco Benvenuti, Brigitte Granel, Elena Rezus, Leila Caillault, Sophie Blaise, Cristiana Sieiro Santos, Fabio Cacciapaglia, Roberto Giacomelli, Rossella De Angelis, Serena Guiducci, Duygu Temiz Karadag, Gabriella Szűcs, Luca Idolazzi, Gábor Kumánovics, Florenzo Iannone, Maurizio Cutolo, Gianluca Moroncini, Valeria Riccieri, Nicoletta Del Papa, Elisabetta Zanatta, Oliver Distler, Masataka Kuwana, Carlo Selmi, Maria De Santis +52 morewiley +1 more sourceComplement Activation Linked to Type II Interferon Signaling in Still Disease
Arthritis &Rheumatology, EarlyView.Objective
Still disease (SD) is an autoinflammatory syndrome characterized by innate immune dysregulation. Although complement can drive inflammation, its involvement in SD remains to be defined. Thus, we aimed to assess complement activation in SD. Methods
Complement was assessed using transcriptomic, proteomic, and in vitro approaches. RNA sequencing Freya M. C. H. Huijsmans, Tabea Thalheim, Alejandra Bodelón, Greta Rogani, Lyanne J. P. M. Sijbers, Remco G. A. Erkens, Aafke de Ligt, Rianne Scholman, Aron Brinker, Gisella B. Beretta, Nienke M. Ter Haar, Thomas Vogl, Johannes Roth, Trang T. Duong, Sytze de Roock, Joost F. Swart, Deborah A. Marshall, Susanne M. Benseler, Rae S. M. Yeung, Christoph Kessel, Sebastiaan J. Vastert, Emely L. Verweyen, Jorg van Loosdregt, on behalf of the UCAN CAN‐DU/UCAN CURE Consortia and the One Child Every Child Initiative, Adam Huber, Bianca Lang, Chelsea DeCoste, Elizabeth Stringer, Suzanne Ramsey, Alan Rosenberg, Kate Neufeld, Mehul Jariwala, Tristan Kerr, Alexander Mosoiu, Alisa Rachlis, Amy Xu, Arthur Cheng, Brenleigh Jebb, Brian Feldman, Bruno Pereira, Deborah Levy, Dilan Dissanayake, Elizaveta Limenis, Evelyn Rozenblyum, Harper Cheng, Jennifer Ji Young Lee, Lynn Spiegel, Rayfel Schneider, Ronald Laxer, Ruud Verstegen, Shirley Tse, Andrea Human, David Cabral, Herman Tam, Jaime Guzman, Kim Morishita, Kristin Houghton, Lori Tucker, Mercedes Chan, Ross Petty, Tommy Gerschman, Annet van Royen‐Kerkhof, Berent Prakken, Erika Van Nieuwenhove, Marc Jansen, Nico Wulffraat, Ciarán Duffy, Nadia Luca, Roman Jurencak, Tala El Tal, Claire LeBlanc, Gaëlle Chédeville, Piya Lahiry, Rosie Scuccimarri, Sarah Campillo, Clare Hutchinson, Daniah Basodan, Dax G Rumsey, Hon Yan Ng, Jeanine McColl, Lillian Lim, Tara McGrath, Danielle Brinkman, Petra Hissink Muller, Elizabeth Legger, Wineke Armbrust, Ellen Schatorje, Esther Hoppenreijs, Elodie Boudes, Gillian Currie, Heinrike Schmeling, Muhammed Dhalla, Nicole Johnson, Paivi Miettunen, Ravneet Sran, Rebeka Stevenson, Erkan Demirkaya, Jonathan Park, Roberta Berard, Giske Biesbroek, Mariken Gruppen, Gordon Soon, Joseph Cafazzo, Liane Heale, Michelle Batthish, Tania Cellucci, Lily Lim, Maarten IJzerman, Marinka Twilt, Marleen Verkaaik, Philomine van Pelt, Sylvia Kamphuis, Michelle Kip, Nicholas Blanchette, Paul Dancey, Regina de Geus +115 morewiley +1 more sourcePersistent Interleukin‐18 Fuels Expansion of CD38+HLA‐DR+CD8+ T Cells in Still Disease and Macrophage Activation Syndrome
Arthritis &Rheumatology, EarlyView.Objective
Still disease (SD) is an autoinflammatory disorder characterized by remarkably high interleukin‐18 (IL‐18) levels. Increasing evidence suggests that adaptive immunity also contributes to its pathogenesis, particularly in refractory courses. Macrophage activation syndrome (MAS), one of SD's most severe complications, is associated with further Greta Rogani, Remco G. A. Erkens, Alejandra Bodelón, Tim R. Mocking, Marein T. M. Putmans, Freya M. C. H. Huijsmans, Lyanne J. P. M. Sijbers, Aafke M. De Ligt, Maurice J. H. Van Haaren, Rianne C. Scholman, Noël M. M. Dautzenberg, Joyce I. Meesters‐Ensing, Martina Rossano, Laura Porretti, Stefan Nierkens, Francesca S. Minoia, Sebastiaan J. Vastert, Jorg van Loosdregt +17 morewiley +1 more sourceOptimizing Efficacy to Safety Ratio of Glucocorticoids in Rheumatoid Arthritis Models by Leveraging Peroxisome Proliferator–Activated Nuclear Receptor‐α Agonism
Arthritis &Rheumatology, EarlyView.Objective
Glucocorticoids remain essential therapies for immune and inflammatory diseases such as rheumatoid arthritis (RA) but are notorious for their metabolic side effects. Given the anti‐inflammatory and metabolically favorable actions of peroxisome proliferator–activated nuclear receptor (PPAR) agonists, we investigated whether PPARα agonism could Lisa L. Koorneef, Elisabeth Gilis, Dorien Clarisse, Daria Fijalkowska, Sara Dufour, Julie Coudeneys, Bert Luyckx, Annick Verhee, Jonathan Thommis, Candice Vanden Bussche, Ulf Müller‐Ladner, Elena Neumann, Matthias Kerkhofs, Guillaume Planckaert, Simon Devos, Leander Meuris, Dirk Elewaut, Karolien De Bosscher +17 morewiley +1 more sourceHuman Monocytic Models Reveal Genotype‐Dependent Inflammatory Programs in VEXAS Syndrome
Arthritis &Rheumatology, EarlyView.Objective
VEXAS syndrome is a severe X‐linked autoinflammatory disorder caused by somatic mutations in ubiquitin‐like modifier activating enzyme 1 (UBA1), with clinical outcomes that vary by UBA1 genotype. We aimed to elucidate genotype‐specific inflammatory programs and identify potential therapeutic targets.Kana Higashitani, Tatsuma Ban, Yohei Kirino, Go R. Sato, Soichiro Adachi, Yuki Iizuka, Kayo Harita, Ayaka Maeda, Osamu Ohara, Hideaki Nakajima, Tomohiko Tamura +10 morewiley +1 more sourceImpact of Dual Interleukin‐17A and Interleukin‐17F Inhibition With Bimekizumab on Inflammatory and Structural Lesions in Axial Spondyloarthritis: Magnetic Resonance Imaging and Radiographic Outcomes From Two Phase 3 Studies and Their Open‐Label Extension
Arthritis &Rheumatology, EarlyView.Graphical Abstract Objective
To evaluate the impact of bimekizumab, a dual interleukin (IL)‐17A and IL‐17F inhibitor, on sacroiliac joints (SIJ) and spine inflammation/structural damage in axSpA using magnetic resonance imaging (MRI) scans/radiographs from the phase 3 studies BE MOBILE 1 (non‐radiographic axSpA [nr‐axSpA]) and 2 (radiographic axSpA [r ...Walter P. Maksymowych, Sofia Ramiro, Denis Poddubnyy, Xenofon Baraliakos, Robert G. W. Lambert, Ute Massow, Tom Vaux, Chetan Prajapati, Alexander Marten, Natasha de Peyrecave, Mikkel Østergaard +10 morewiley +1 more source