Results 171 to 180 of about 24,656 (260)
The Nuclear Receptor Testicular Receptor 4 Orchestrates Cytoskeletal Organization in a G Protein Subunit Alpha 12/Rho‐Associated Protein Kinase–Dependent Manner to Promote Myofibroblast Differentiation and Tissue Fibrosis in Systemic Sclerosis
Arthritis &Rheumatology, EarlyView.Objective
Members of the superfamily of nuclear receptors have been implicated in inflammatory processes and pathologic tissue remodeling and have emerged as attractive targets for pharmaceutical intervention. However, the role of testicular receptor 4 (TR4; or Nr2c2) in fibroblast activation and rheumatologic diseases has not yet been investigated ...Yun Zhang, Lichong Shen, Junhui Zheng, Gisela Baur, Dilidaer Yasen, Honglin Zhu, Yi‐Nan Li, Xianyi Meng, Thuong Trinh‐Minh, Tim Filla, Debomita Chakraborty, Andrea‐Hermina Györfi, Christina Bergmann, Adam Reich, Alexander Kreuter, Georg Schett, Jörg H. W. Distler +16 morewiley +1 more sourceDnmt3a Mutations Limit Normal and Autoreactive CD4+ T Follicular Helper Responses and Attenuate T Cell–Driven Joint Inflammation
Arthritis &Rheumatology, EarlyView.Objective
Somatic DNMT3A mutations are the most common drivers of clonal hematopoiesis in patients with rheumatoid arthritis (RA) and have been associated with seropositive disease and increased markers of inflammation. These mutations are predominantly hypomorphic or dominant‐negative, reducing DNMT3A function.Yunbing Shen, Sanjaykumar Boddul, Zhaojun Li, Zsolt Kasza, Marlene Schülein, Bruno Raposo, Karine Chemin, Per‐Johan Jakobsson, Alexander Espinosa, Lars Klareskog, Fredrik Wermeling +10 morewiley +1 more sourceGenetic and Population Analyses Implicate Thyroid‐Related Regulation of RNF144B in Chondrocalcinosis
Arthritis &Rheumatology, EarlyView.Objective
Chondrocalcinosis, characterized by calcium crystal deposition within articular cartilage, affects 5% to 15% of the general population and has recently been identified as an osteoarthritis risk factor. However, its biologic pathways remain unclear.Yahong Wu, Yanning Xu, Paul C. Okoro, Sirine Saafi, Jard de Vries, Xiaoyi Qi, Edwin H. G. Oei, Sita Bierma‐Zeinstra, Trudy Voortman, David Felson, Joyce B. J. van Meurs, Layal Chaker, J. Mark Wilkinson, Michelle S. Yau, Jessica Bertrand, Cindy G. Boer +15 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 source